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*
Melbourne Tumor Biology Branch, Ludwig Institute for Cancer Research, Melbourne, Victoria, Australia;
Molecular Genetics and Development Group, Institute of Reproduction and Development, Monash University, Melbourne, Victoria, Australia;
Christchurch Hospital, Christchurch, New Zealand; and
§
Austin Research Institute, Melbourne, Victoria, Australia
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Abstract |
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 Top Abstract IntroductionMaterials and MethodsResultsDiscussionReferences |
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, and IL-4, CD34+ progenitors gave rise to a
population of large, immature DC expressing CD1a and CD11b but lacking
CD14, CD80, CD83, CD86, and CMRF44. During the next 2 wk, this
population spontaneously matured into nonadherent,
CD1alow/-, CD11blow/-, CD14-,
CD80+, CD83+, CD86+,
CMRF44+ DC with high allostimulatory activity in the MLR.
To examine which factors influenced this maturation, 25 different
cytokines or factors were added to the immature DC culture. Only type I
IFNs ( or ß) accelerated this maturation in a dose-dependent
manner, so that after only 3 days the majority of large cells acquired
the morphology, phenotype, and function characteristics of mature DC.
Furthermore, supernatants from cultures containing spontaneously
maturing DC revealed low levels of endogenous IFN production. Because
of the similarity of the activation of DC in our culture system with
the phenotypic and functional changes observed during Langerhans cells
activation and migration in vivo, we investigated the effect of IFN-
on human Langerhans cell migration. IFN- also activated the
migration of human split skin-derived DC, demonstrating that this
effect was not limited to DC derived in vitro from hemopoietic
progenitor cells. DC activation by type I IFNs represents a novel
mechanism of immunomodulation by these cytokines, which could be
important during antiviral responses and autoimmune
reactions. |
Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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These earlier in vitro studies of DC development and maturation were performed in the presence of FCS or human serum (HS). The presence of irrelevant Ags, undefined growth factors, and potential infectious agents in serum represent major impediments to the use of these DC in human disease, leading us to investigate cytokine and culture conditions required for the serum-free production of these cells.
We have previously described a serum-free culture model to produce human DC from adult CD34+ hemopoietic progenitor cells (10). Progenitor cells purified from leukapheresis harvests of cancer patients with mobilizing treatments, from the bone marrow of rib fragments of patients with lung cancer undergoing thoracotomy, and from normal bone marrow donors were compared. These progenitor cells of various sources gave rise to similar DC cultures. The study reported the accumulation of a large-size, CD1a+CD11b+CD14- population of immature DC differentiating from myeloid CD33+ precursor cells after 13 to 15 days in culture. No markers associated with activated DC (CD80, CD83, CD86) were expressed before day 15. During the following 14 days, this large-size population spontaneously matured into DC that displayed an activated phenotype (HLA-A,B,Cbright, HLA-DRbright, CD80+, CD83+, and CD86+). CD1a and CD11b expression was gradually lost. At day 28, mature and immature DC stages coexisted in cultures. However, CD1a+CD11b+ DC sorted at day 13 matured homogeneously, and there was no evidence for a direct precursor of mature DC in the small-size CD1a- population. Further, extending the observation period to 37 days showed that all large cells finally acquired the activated phenotype. This study suggested that in serum-free cultures DC differentiate and mature in an asynchronous manner. Homogeneity of phenotypes was achieved by allowing more time for differentiation or by sorting precursors of a defined stage of differentiation. These activated DC were shown to be potent APCs (10). Characterizing the differentiation and activation of DC revealed close similarities with the phenotypic and functional changes occurring during Langerhans cell activation and migration (11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24). This system has now enabled us to more precisely define the cytokines that regulate DC development. Type I IFNs were the only molecules of a large number studied that were capable of inducing DC maturation and activation. This study, therefore, identifies a novel mechanism for the immunomodulatory effects of type I IFNs, which is important for further understanding the cytokine regulation of DC function.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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The serum-free medium X-Vivo 20 was purchased from BioWhittaker (Walkersville, MD). Cell lines were maintained in RPMI 1640 (Trace Biosciences, Melbourne, Australia) supplemented with 20 mM HEPES, 60 mg/L penicillin G, 12.6 mg/L streptomycin, 2 mM L-glutamine, 1% nonessential amino acids, and 10% heat-inactivated FCS (CSL, Melbourne, Australia).
Recombinant human cytokines, Abs, and peptides
The following cytokines were added to DC cultures: TNF- (20
ng/ml) (R&D Systems, Minneapolis, MN); GM-CSF (40 ng/ml;
Schering-Plough, Sydney, Australia), IL-4 (500 U/ml, Schering-Plough,
Kenilworth, NJ), IFN-2a (10–1000 U/ml, Roferon-A; Roche Products,
Sydney, Australia), IFN-8 (10–1000 U/ml, (Ciba-Geigy, Basel,
Switzerland), and IFN-ß (10–1000 U/ml, Berlex Biosciences, Richmond,
CA). The cytokines used for screening experiments were: IL-1 (10
ng/ml, Dr. I. Campbell, Department of Medicine, Royal Melbourne
Hospital, Melbourne, Australia); IL-1ß (100 pg/ml; R&D Systems); IL-2
(100 U/ml, PreproTech, Rocky Hill, NJ); IL-3 (100 ng/ml, Dr. G.
Begley, The Walter and Eliza Hall Institute (WEHI), Melbourne,
Australia); IL-4 (1000 U/ml, Schering-Plough, Kenilworth, NJ); IL-6 (20
ng/ml, Dr. R. Simpson, Ludwig Institute for Cancer Research (LICR),
Melbourne, Australia); IL-7 (20 ng/ml, Serotec, Oxford, U.K.); IL-8
(100 ng/ml, Dr. I. Campbell, Royal Melbourne Hospital); IL-10 (100
U/ml, Schering-Plough, Kenilworth, NJ); IL-12 (10 ng/ml, R&D Systems);
IL-13 (20 ng/ml; PreproTech, London, U.K.); GM-CSF (50 ng/ml, Dr. G.
Begley, WEHI); TNF- (100 ng/ml, R&D Systems); TGF-ß (1 ng/ml, Dr.
S. Chandler, LICR), IFN-2a (1000 U/ml, Roche Products, DeeWhy,
Australia); IFN-
(1000 U/ml, Boehringer, Ingelheim, Germany);
platelet-derived growth factor (PDGF; 20 ng/ml, Dr. R.
Whitehead, LICR); vascular endothelial growth factor (VEGF; 10
ng/ml, Dr. S. Stacker, LICR); insulin-like growth factor (IGF)-1
(LR3) (50 ng/ml, Dr. R. Whitehead, LICR); IGF-1 (50 ng/ml, Dr.
R. Whitehead, LICR); leukemia inhibitory factor (LIF; 1000 U/ml, Dr. N.
Nicola, WEHI); stem cell factor (SCF; 100 ng/ml, Dr. G. Begley,
WEHI); FLT-3L (40 ng/ml, Genzyme Corp., Boston, MA); LPS serotype
0111:B4 (100 ng/ml, Sigma, St. Louis, MO); BSA (1%, Sigma); HS (10%,
normal donors), and HS-LPS (10%, normal donors, serum filtered with
Zetapor filter (Cuno-Life Sciences Division, Meriden, CT) to remove
LPS). The following commercial mAbs were purchased: FITC-conjugated
IgG1 isotype control, OKT6 (anti-CD1a), phycoerythrin-conjugated T4
(anti-CD4), and BB-1 (anti-CD80/B7/BB1) from Serotec; 5C3
(anti-CD40) and IT2.2 (anti-CD86/B70/B7-2) from PharMingen (San
Diego, CA); and FITC-conjugated sheep anti-mouse mAb (Silenus,
Boronia, Australia). The following mouse Ab were kindly provided
by Dr. A. Boyd (WEHI): IAG-11 negative control, W6/32,
anti-HLA-A,B,C; Ia, anti HLA-DR; OKM-1, anti-CD11b; FMC 17,
anti-CD14. HB15a, anti-CD83, was a gift from Dr. T. Tedder,
Duke University Medical Center (Durham, NC). CMRF44 were obtained from
Dr. D. Hart, Department of Haematology, Christchurch Hospital (25).
Cell sources and cell lines
Bone marrow and leukapheresis harvest samples were obtained from normal donors and patients of the Department of Medical Oncology and Clinical Haematology, Royal Melbourne Hospital, Melbourne, Australia. Patients with lymphoma or solid tumors received stem cell-mobilizing chemotherapy and granulocyte colony-stimulating factor (G-CSF) as part of their treatment. Rib segments removed during thoracotomy from patients were obtained from the Department of Thoracic Surgery, Austin and Repatriation Medical Center. Informed consent was obtained. Protocols were approved by the Ethics Committee and conformed to the guidelines of the National Health and Medical Research Council of Australia.
Cell separation and DC cultures
Samples were separated on Ficoll-Hypaque (Pharmacia Biotech, Uppsala, Sweden); RBC were lysed using NH4Cl, and CD34+ cells were separated with the MACS CD34 progenitor cell isolation kit (Miltenyi Biotech, Sunnyvale, CA) following the manufacturer’s instructions. Cells (106/ml, 4 x 106/ml) were cultured in 100 µl of X-Vivo 20 with cytokines in 96-well microcultures (Nunc, Roskilde, Denmark) or in 250 µl of medium in 24-well plates (Nunc); 50 to 100% fresh medium and cytokines were added twice weekly. Proliferating, crowded cultures were split or transferred with an Eppendorf pipette into progressively larger tissue culture plates (48-well plates (Falcon, Franklin Lakes, NJ), 24-well plates (Nunc), and 12-well plates (Flow Laboratories, McLean, VA)). The CD34- fraction was used for HLA typing (Victorian Tissue Typing Service, Royal Melbourne Hospital).
Morphology, flow cytometry, and FACS
Cytocentrifuge preparations were performed by applying 104 cells to glass slides spinning for 10 min at 300 rpm (Cytospin 2, Shandon, Pittsburgh, PA). The slides were air dried and stained with May-Grunwald/Giemsa. Cells for flow cytometry were resuspended in PBS + 10% HS, labeled with the primary Abs, washed, and labeled with the secondary Ab. Cells were fixed in PBS/2% formaldehyde/0.01% sodium azide/1% BSA. The immunophenotype was determined using a FACScan flow cytometer (Becton Dickinson, Franklin Lakes, NJ). Fluorescence-activated cell sorting (FACS) was performed on either a FACStarPlus or a modified FACS II flow cytometer.
Mixed leukocyte reaction (MLR)
After irradiation (3000 rad), stimulator cells from DC cultures were plated in triplicate over a range of concentrations (10,000–3,000–1,000–300 per well) and overlaid with 105 allogeneic PBMC. PBMC of healthy laboratory volunteers were used as responders. Cells were cultured for 5 days in RPMI with 10% HS in 96-well round-bottom plates. After 5 days, cells were incubated with 1 µCi/well [3H]thymidine (DuPont, Sydney, MA) for 20 h, transferred onto a glass fiber filter (Wallac, Turku, Finland), and [3H]thymidine incorporation into DNA was measured using an LKB 1205 Betaplate scintillation counter (Wallac).
Migration of skin-derived DC
Split skin samples were obtained from the Department of Plastic
Surgery, Austin and Repatriation Medical Centre, cut into paired pieces
of equal size (1–2 cm2), and cultured in X-Vivo 20 (2.5
ml, 6-well plate). Three thousand units per milliliter of IFN-2a was
added into one culture of each paired experiment. Two to three
replicate paired experiments were performed for each donor skin sample.
Numbers of migrating DC were assessed 12 hourly by morphologic criteria
using a hemocytometer. Every 24 h, cells were harvested for FACS
analysis and skin samples were transferred into fresh medium.
Assay for the antiviral activity of IFN
The antiviral activity of IFN was determined by cytopathic effect reduction assay using WISH cells (American Type Culture Collection (ATCC), Manassas, VA) as the target cells and Semliki forest virus (ATCC) as the challenge virus, as previously described (26). The amount of IFN in IU/ml was calculated by comparing the titer of a sample with that of the international reference standard, Ga 23901532 (National Institutes of Health, Bethesda, MD).
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Results |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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In serum-free cultures of human CD34+ progenitor
cells, two stages of DC differentiation were observed. In the early
phase of culture, (10–16 days), a population of large, adherent,
Langerhans-like cells developed. These cells were
CD1a3+, CD11b3+, CD14-,
CD80-, CD83-, CD86-,
HLA-A,B,C+, and HLA-DR+ cells (Fig. 1
) and possessed a low allostimulatory
capacity (Fig. 2). During the next 2 wk
(late phase, days 17–28), this population spontaneously matured into
nonadherent APC with up-regulation of HLA-A,B,C, HLA-DR, costimulatory
molecules (CD80, CD86), and DC lineage-associated Ags (CD83, CMRF44)
(Fig. 1). Simultaneously, down-regulation of CD11b and CD1a was seen
(Fig. 1). The loss of these Ags was slow and was complete between days
28 and 40. No Birbeck granules were found in activated DC. This late
phase (d14–28), now referred to as phenotypic maturation, was
associated with a loss of adherence to plastic. The Ag-presenting
capacity of cells from unsorted cultures was examined on days 14 and 28
(Fig. 2). Direct comparison of cells from both time points was possible
because the same donor of responder cells was used within the paired
experiments. Figure 2 shows the significantly increased allostimulatory
capacity of day 28 DC cultures compared with day 14 DC cultures. We
have previously shown that mature DC in these cultures were derived
solely from the CD1a3+, CD11b3+ population.
These cells were capable of transient adherence to plastic and
developed into nonadherent, CD11blow/-, CD14+,
CD862+, CMRF44+ DC. IL-4 was not required for
this final maturation. Cell sources included leukapheresis harvests and
bone marrow samples, predominantly of cancer patients but also normal
bone marrow. No differences in differentiation and activation of
progenitor-derived DC from different sources were observed (10).
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To determine whether addition of exogenous cytokines could
accelerate DC maturation and to identify those endogenous factors that
might be acting, we screened a variety of cytokines for their effects
on DC phenotype in serum-free cultures. HLA-DR and/or CD86
up-regulation were used as markers of maturation. For this assay,
cytokines were used at a concentration previously found to be active in
other systems (see Materials and Methods). Cytokines were
added on day 14, and cultures were analyzed by flow cytometry for the
presence of activated (HLA-DRbright, CD86+) DC
on day 17. Each set of experiments (n = 23) included
control cells grown in standard conditions in GM-CSF, TNF-, and
IL-4. The percentage of activated DC in these control cultures on day
17 was referred to as 100%. SDs were calculated for all experiments to
control for the variations between individual experiments. Twice the
mean of all SD was used to define the no-difference interval (gray) in
Figure 3. Only normal HS, HS filtered
through a Zetapor filter to remove LPS (HS-LPS), and IFN-2a were
capable of increasing the percentage of activated DC above 2 SD of the
control.
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To determine whether other type I IFNs could also accelerate DC
maturation, IFN-2a, IFN-8, and IFN-ß were added to cultures
containing GM-CSF, IL-4, and TNF-. Each of the three IFNs had a
similar capacity to up-regulate HLA-A,B,C, CD80, and CD86 and to
down-regulate CD1a and CD11b expression on the large cell population
(n = 3). These changes occurred within 3 days and were
concentration dependent (Fig. 4).
Furthermore, up-regulation of HLA-DR, CD83, and CMRF44 expression was
observed in response to IFN-2a (shown for CD83 in Fig. 5). Cell numbers and percentages of large
cells in culture did not significantly change during the 3 days of
exposure to IFN-. There was no evidence of increased cell death of
large cells during this period.
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could also activate DC function, the
allostimulatory capacity of DC-containing bulk cultures was compared
with or without a 3-day exposure to IFN-2a. Figure 6A shows the results of six
individual experiments. Cultures were split on day 14, and IFN-2a
(1000 U/ml) was added daily for 3 days into one-half of the cultures.
Cultures exposed to IFN-2a contained 23 ± 3.4%
CD86+ DC, and these cells showed a significantly increased
allostimulatory capacity (*p < 0.05). Cultures without
IFN- contained 9 ± 1.5% CD86+ DC on day 17. These
results were confirmed by an MLR using DC sorted on day 18 according to
their high forward and side scatter characteristics (24). DC exposed to
IFN-2a for 3 days were more stimulatory than control DC (Fig. 6B).
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and IFN-
To investigate whether IFN- could act alone or required TNF-
to induce DC maturation, cultures were washed on day 14 and continued
until day 17 in serum-free medium containing GM-CSF and IL-4, without
or with TNF- (20 ng/ml, standard conditions), IFN-, or
both. IFN- alone did not enhance DC maturation as compared
with standard conditions. Both TNF- and IFN- were required for
optimal maturation, as shown in Table I.
Thus, the enhancement of DC activation by IFN- under serum-free
conditions required the presence of TNF-.
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production in serum-free cultures of DCSince type I IFNs were the only cytokines that could stimulate DC maturation, it appeared likely that autocrine or paracrine production of IFN was responsible for DC maturation in our serum-free cultures. This hypothesis was tested by assaying culture supernatants for IFN activity. Supernatants were collected at different times between days 14 and 30. IFN activity corresponding to 12 ± 2 IU/ml (range, 8–25 IU/ml) was detected in 10 samples in cultures from six patients. In supernatants from cultures from five other patients, IFN-like activity was not detectable. These data suggest that type I IFNs can be produced by the cells in these cultures and may act as autocrine or paracrine factors to regulate the final stages of DC maturation.
IFN- and skin-derived DC
The similarity of phenotype and activation patterns of
progenitor-derived DC and Langerhans cells led us to investigate
whether type I IFNs were capable of activating skin-derived DC as well.
Paired, split skin samples of similar sizes (1–2 cm2) were
floated in serum-free tissue culture medium, and cells migrating into
the liquid phase were compared by assessing numbers of
CD1a+CD80+CD83+ cells with typical
dendritic morphology. Cells were counted every 12 h and
harvested for FACS analysis every 24 h, at which time the skin was
transferred into fresh medium. In the presence of IFN- (3000 U/ml),
increased numbers of migrating DC were observed in 5 of 9
patients (Table II).
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Three different pathways have been described according to their
intermediate (early) stages, which result in myeloid DC of similar
phenotype. These include CD14+ monocytic cells (7, 10),
CD14-CD1a+ Langerhans cells (27, 28, 29), and
CD14-CD1a- peripheral blood-derived DC (6).
Under the conditions described here, CD34+ cells
differentiated to an intermediate stage, which is CD14-
and CD1a+. This is consistent with the Langerhans cell
phenotype. As with freshly isolated Langerhans cells (30), these early
DC in serum-free cultures were characterized by intermediate HLA-A,B,C
and HLA-DR expression, high expression of CD1a, expression of CD11b,
and the lack of accessory molecules (CD80, CD86) as well as
DC-associated molecules CD83 and CMRF44. In the presence of TNF-,
these immature DC took another 14 days to acquire the phenotypic and
functional characteristics typical of activated DC. The phenotypic and
functional changes observed during this process were similar to those
seen in other studies and involved the up-regulation of HLA-A,B,C,
HLA-DR (18), CD80, CD86 (19, 20), CD83, and CMRF44, down-regulation of
CD1a and CD11b (18), and functional maturation (7, 10) into highly
allostimulatory cells. In parallel, cells lost their ability to adhere
to plastic and became nonadherent round cells with a corona of thin
dendrites.
The spontaneous maturation in these serum-free cultures suggested that
the production of autocrine or paracrine factors might be involved in
this process. We therefore screened a number of cytokines and other
molecules for their action in this system. Apart from HS, only type I
IFNs ( or ß) were capable of accelerating maturation, so that
within 3 days a majority of the large-size cells in culture expressed
CD80, CD83, and CD86 and started to down-regulate CD1a and CD11b. This
effect of IFNs added into cultures containing GM-CSF, IL-4, and TNF-
was concentration dependent in a range between 10 and 1000 U/ml and was
similar for three different type I IFNs (2a, 8, and ß) (Fig. 4
). In parallel with the phenotypic changes, DC exposed to IFN- had
increased T cell stimulatory capacity. Both IFN- and TNF- were
required for DC activation between days 14 and 17. Synergy of TNF-
and IFN on HLA class I expression has been previously reported at the
level of transcriptional regulation (31). The nature of the effector in
HS activating DC remains unknown. It has recently been shown that HS
contains soluble CD14, which forms complexes with LPS and as a complex
can activate CD14- DC (32). Therefore, these results also
provide an explanation as to why LPS in the absence of serum did not
activate our CD14- DC.
We have shown that IFN-like activity was produced in most spontaneously
maturing serum-free DC cultures. Since autocrine production of IFN-
can cause significant biologic effects even in the absence of
detectable activity in the supernatant (26), we regard the presence of
measurable activity in cultures from 6 of 11 patients as significant.
The clear effect of exogenously added IFN-, the low level production
of IFN-like activity in the cultures, and the prolonged period of
immaturity, even in the presence of a high dose of TNF-, all suggest
that type I IFNs provide a necessary signal for the induction of DC
maturation and activation.
In addition to the effects of IFN- on in vitro-derived DC, we showed
that IFN- activated migration of resident DC from split skin samples
floating in serum-free medium. These results suggest that the adherent,
immature DC in our serum-free cultures are similar to skin-derived DC
in their response to type I IFN as well as in phenotype.
These experiments open a new perspective on the events involved in DC
maturation and activation, showing that type I IFN can enhance the
effect of TNF- in the induction of this process. This suggests that
in addition to the multiple immunomodulatory effects, type I IFNs may
also regulate immune responses at the level of the APC. Type I IFNs
have a well-established role in the response to infections with viruses
(33, 34, 35). Immunomodulatory effects include the promotion of Th1
responses by inhibition of IL-4 and IL-5 secretion (36, 37), increase
in IFN--producing cells (38), and effects on IgG production (13).
Our studies show a novel mechanism, which is that type I IFNs also
mediate effects by inducing maturation and activation of DC. This may
help to explain the autoimmune phenomena associated with the use
of IFN in hepatitis and cancer patients (33, 39, 40, 41). It may also
provide an additional mechanism for the anticancer effects of IFN-
in a variety of tumors (42, 43, 44, 45, 46, 47).
Importantly, these results may have an impact on clinical strategies
for developing cancer vaccines. While IFNs are being used as adjuvant
therapy for cancer and as antiviral therapy, the effect of IFNs on DC
function has not previously been defined. IFN- might therefore be a
useful candidate as a vaccine adjuvant in clinical trials using tumor
Ags as vaccines. Furthermore, this serum-free system should assist the
further study of events associated with DC activation, as well as
providing clinical opportunities for using IFN-activated DC as cellular
adjuvants.
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Acknowledgments |
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Footnotes |
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2 Address correspondence and reprint requests to Dr. Thomas Luft, Ludwig Institute Oncology Unit, Austin and Repatriation Medical Center, Studley Road, Heidelberg, Victoria 3084, Australia.
3 Abbreviations used in this paper: DC, dendritic cells; GM-CSF, granulocyte macrophage-CSF; HS, human serum.
Received for publication December 12, 1997. Accepted for publication April 14, 1998.
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References |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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 B. Zeng, H. Li, Y. Liu, Z. Zhang, Y. Zhang, and R. Yang Tumor-Induced Suppressor of Cytokine Signaling 3 Inhibits Toll-like Receptor 3 Signaling in Dendritic Cells via Binding to Tyrosine Kinase 2 Cancer Res., July 1, 2008; 68(13): 5397 - 5404. [Abstract] [Full Text] [PDF]
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V. Veckman and I. Julkunen Streptococcus pyogenes activates human plasmacytoid and myeloid dendritic cells J. Leukoc. Biol., February 1, 2008; 83(2): 296 - 304. [Abstract] [Full Text] [PDF]
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U. Johansson, L. Walther-Jallow, A. Smed-Sorensen, and A.-L. Spetz Triggering of Dendritic Cell Responses after Exposure to Activated, but Not Resting, Apoptotic PBMCs J. Immunol., August 1, 2007; 179(3): 1711 - 1720. [Abstract] [Full Text] [PDF]
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J. B. Swann, Y. Hayakawa, N. Zerafa, K. C. F. Sheehan, B. Scott, R. D. Schreiber, P. Hertzog, and M. J. Smyth Type I IFN Contributes to NK Cell Homeostasis, Activation, and Antitumor Function J. Immunol., June 15, 2007; 178(12): 7540 - 7549. [Abstract] [Full Text] [PDF]
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M. A. Nolte, S. LeibundGut-Landmann, O. Joffre, and C. R. e Sousa Dendritic cell quiescence during systemic inflammation driven by LPS stimulation of radioresistant cells in vivo J. Exp. Med., June 11, 2007; 204(6): 1487 - 1501. [Abstract] [Full Text] [PDF]
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E. M. Behrens, U. Sriram, D. K. Shivers, M. Gallucci, Z. Ma, T. H. Finkel, and S. Gallucci Complement Receptor 3 Ligation of Dendritic Cells Suppresses Their Stimulatory Capacity J. Immunol., May 15, 2007; 178(10): 6268 - 6279. [Abstract] [Full Text] [PDF]
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H. J. Kim, J. S. Yang, S. S. Woo, S. K. Kim, C.-H. Yun, K. K. Kim, and S. H. Han Lipoteichoic acid and muramyl dipeptide synergistically induce maturation of human dendritic cells and concurrent expression of proinflammatory cytokines J. Leukoc. Biol., April 1, 2007; 81(4): 983 - 989. [Abstract] [Full Text] [PDF]
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 W. A. Derbigny, S.-C. Hong, M. S. Kerr, M. Temkit, and R. M. Johnson Chlamydia muridarum Infection Elicits a Beta Interferon Response in Murine Oviduct Epithelial Cells Dependent on Interferon Regulatory Factor 3 and TRIF Infect. Immun., March 1, 2007; 75(3): 1280 - 1290. [Abstract] [Full Text] [PDF]
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R. Romieu-Mourez, M. Solis, A. Nardin, D. Goubau, V. Baron-Bodo, R. Lin, B. Massie, M. Salcedo, and J. Hiscott Distinct Roles for IFN Regulatory Factor (IRF)-3 and IRF-7 in the Activation of Antitumor Properties of Human Macrophages Cancer Res., November 1, 2006; 66(21): 10576 - 10585. [Abstract] [Full Text] [PDF]
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J. S. Yount, T. A. Kraus, C. M. Horvath, T. M. Moran, and C. B. Lopez A Novel Role for Viral-Defective Interfering Particles in Enhancing Dendritic Cell Maturation J. Immunol., October 1, 2006; 177(7): 4503 - 4513. [Abstract] [Full Text] [PDF]
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M. Alsharifi, M. Regner, R. Blanden, M. Lobigs, E. Lee, A. Koskinen, and A. Mullbacher Exhaustion of Type I Interferon Response following an Acute Viral Infection. J. Immunol., September 1, 2006; 177(5): 3235 - 3241. [Abstract] [Full Text] [PDF]
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J. Louten, N. van Rooijen, and C. A. Biron Type 1 IFN Deficiency in the Absence of Normal Splenic Architecture during Lymphocytic Choriomeningitis Virus Infection. J. Immunol., September 1, 2006; 177(5): 3266 - 3272. [Abstract] [Full Text] [PDF]
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C. J. Montoya, H.-B. Jie, L. Al-Harthi, C. Mulder, P. J. Patino, M. T. Rugeles, A. M. Krieg, A. L. Landay, and S. B. Wilson Activation of Plasmacytoid Dendritic Cells with TLR9 Agonists Initiates Invariant NKT Cell-Mediated Cross-Talk with Myeloid Dendritic Cells J. Immunol., July 15, 2006; 177(2): 1028 - 1039. [Abstract] [Full Text] [PDF]
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C. B. Lopez, J. S. Yount, T. Hermesh, and T. M. Moran Sendai Virus Infection Induces Efficient Adaptive Immunity Independently of Type I Interferons J. Virol., May 1, 2006; 80(9): 4538 - 4545. [Abstract] [Full Text] [PDF]
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P. Aichele, H. Unsoeld, M. Koschella, O. Schweier, U. Kalinke, and S. Vucikuja Cutting edge: CD8 T cells specific for lymphocytic choriomeningitis virus require type I IFN receptor for clonal expansion. J. Immunol., April 15, 2006; 176(8): 4525 - 4529. [Abstract] [Full Text] [PDF]
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C. B. Lopez, J. S. Yount, and T. M. Moran Toll-like receptor-independent triggering of dendritic cell maturation by viruses. J. Virol., April 1, 2006; 80(7): 3128 - 3134. [Full Text] [PDF]
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C. Havenar-Daughton, G. A. Kolumam, and K. Murali-Krishna Cutting Edge: The Direct Action of Type I IFN on CD4 T Cells Is Critical for Sustaining Clonal Expansion in Response to a Viral but Not a Bacterial Infection J. Immunol., March 15, 2006; 176(6): 3315 - 3319. [Abstract] [Full Text] [PDF]
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M. Ahmed, K. L. Brzoza, and E. M. Hiltbold Matrix Protein Mutant of Vesicular Stomatitis Virus Stimulates Maturation of Myeloid Dendritic Cells J. Virol., March 1, 2006; 80(5): 2194 - 2205. [Abstract] [Full Text] [PDF]
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A. N. Honko, N. Sriranganathan, C. J. Lees, and S. B. Mizel Flagellin Is an Effective Adjuvant for Immunization against Lethal Respiratory Challenge with Yersinia pestis Infect. Immun., February 1, 2006; 74(2): 1113 - 1120. [Abstract] [Full Text] [PDF]
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F. Braiteh, C. Boxrud, B. Esmaeli, and R. Kurzrock Successful treatment of Erdheim-Chester disease, a non-Langerhans-cell histiocytosis, with interferon-{alpha} Blood, November 1, 2005; 106(9): 2992 - 2994. [Abstract] [Full Text] [PDF]
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G. A. Kolumam, S. Thomas, L. J. Thompson, J. Sprent, and K. Murali-Krishna Type I interferons act directly on CD8 T cells to allow clonal expansion and memory formation in response to viral infection J. Exp. Med., September 6, 2005; 202(5): 637 - 650. [Abstract] [Full Text] [PDF]
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S.-Y. Dai, R. Nakagawa, A. Itoh, H. Murakami, Y. Kashio, H. Abe, S. Katoh, K. Kontani, M. Kihara, S.-L. Zhang, et al. Galectin-9 Induces Maturation of Human Monocyte-Derived Dendritic Cells J. Immunol., September 1, 2005; 175(5): 2974 - 2981. [Abstract] [Full Text] [PDF]
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T. P. Moran, M. Collier, K. P. McKinnon, N. L. Davis, R. E. Johnston, and J. S. Serody A Novel Viral System for Generating Antigen-Specific T Cells J. Immunol., September 1, 2005; 175(5): 3431 - 3438. [Abstract] [Full Text] [PDF]
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P. Osterlund, V. Veckman, J. Siren, K. M. Klucher, J. Hiscott, S. Matikainen, and I. Julkunen Gene Expression and Antiviral Activity of Alpha/Beta Interferons and Interleukin-29 in Virus-Infected Human Myeloid Dendritic Cells J. Virol., August 1, 2005; 79(15): 9608 - 9617. [Abstract] [Full Text] [PDF]
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A. M. Hahn, L. E. Huye, S. Ning, J. Webster-Cyriaque, and J. S. Pagano Interferon Regulatory Factor 7 Is Negatively Regulated by the Epstein-Barr Virus Immediate-Early Gene, BZLF-1 J. Virol., August 1, 2005; 79(15): 10040 - 10052. [Abstract] [Full Text] [PDF]
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S. Coleman, A. Clayton, M. D. Mason, B. Jasani, M. Adams, and Z. Tabi Recovery of CD8+ T-Cell Function During Systemic Chemotherapy in Advanced Ovarian Cancer Cancer Res., August 1, 2005; 65(15): 7000 - 7006. [Abstract] [Full Text] [PDF]
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M. Rossi and J. W. Young Human Dendritic Cells: Potent Antigen-Presenting Cells at the Crossroads of Innate and Adaptive Immunity J. Immunol., August 1, 2005; 175(3): 1373 - 1381. [Abstract] [Full Text] [PDF]
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S. S. Pejawar, G. D. Parks, and M. A. Alexander-Miller Abortive versus Productive Viral Infection of Dendritic Cells with a Paramyxovirus Results in Differential Upregulation of Select Costimulatory Molecules J. Virol., June 15, 2005; 79(12): 7544 - 7557. [Abstract] [Full Text] [PDF]
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E. M. Bautista, G. S. Ferman, D. Gregg, M. C. S. Brum, M. J. Grubman, and W. T. Golde Constitutive Expression of Alpha Interferon by Skin Dendritic Cells Confers Resistance to Infection by Foot-and-Mouth Disease Virus J. Virol., April 15, 2005; 79(8): 4838 - 4847. [Abstract] [Full Text] [PDF]
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J. M. Curtsinger, J. O. Valenzuela, P. Agarwal, D. Lins, and M. F. Mescher Cutting Edge: Type I IFNs Provide a Third Signal to CD8 T Cells to Stimulate Clonal Expansion and Differentiation J. Immunol., April 15, 2005; 174(8): 4465 - 4469. [Abstract] [Full Text] [PDF]
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C. Asselin-Paturel, G. Brizard, K. Chemin, A. Boonstra, A. O'Garra, A. Vicari, and G. Trinchieri Type I interferon dependence of plasmacytoid dendritic cell activation and migration J. Exp. Med., April 4, 2005; 201(7): 1157 - 1167. [Abstract] [Full Text] [PDF]
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R. A. Prell, B. Li, J. M. Lin, M. VanRoey, and K. Jooss Administration of IFN-{alpha} Enhances the Efficacy of a Granulocyte Macrophage Colony Stimulating Factor-Secreting Tumor Cell Vaccine Cancer Res., March 15, 2005; 65(6): 2449 - 2456. [Abstract] [Full Text] [PDF]
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A. Rolland, L. Guyon, M. Gill, Y.-H. Cai, J. Banchereau, K. McClain, and A. K. Palucka Increased Blood Myeloid Dendritic Cells and Dendritic Cell-Poietins in Langerhans Cell Histiocytosis J. Immunol., March 1, 2005; 174(5): 3067 - 3071. [Abstract] [Full Text] [PDF]
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D. R. Palmer, P. Sun, C. Celluzzi, J. Bisbing, S. Pang, W. Sun, M. A. Marovich, and T. Burgess Differential Effects of Dengue Virus on Infected and Bystander Dendritic Cells J. Virol., February 15, 2005; 79(4): 2432 - 2439. [Abstract] [Full Text] [PDF]
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M. C. Gauzzi, C. Purificato, K. Donato, Y. Jin, L. Wang, K. C. Daniel, A. A. Maghazachi, F. Belardelli, L. Adorini, and S. Gessani Suppressive Effect of 1{alpha},25-Dihydroxyvitamin D3 on Type I IFN-Mediated Monocyte Differentiation into Dendritic Cells: Impairment of Functional Activities and Chemotaxis J. Immunol., January 1, 2005; 174(1): 270 - 276. [Abstract] [Full Text] [PDF]
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E. Barnes, M. Salio, V. Cerundolo, J. Medlin, S. Murphy, G. Dusheiko, and P. Klenerman Impact of Alpha Interferon and Ribavirin on the Function of Maturing Dendritic Cells Antimicrob. Agents Chemother., September 1, 2004; 48(9): 3382 - 3389. [Abstract] [Full Text] [PDF]
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H. Okada, T. Tsugawa, H. Sato, N. Kuwashima, A. Gambotto, K. Okada, J. E. Dusak, W. K. Fellows-Mayle, G. D. Papworth, S. C. Watkins, et al. Delivery of Interferon-{alpha} Transfected Dendritic Cells into Central Nervous System Tumors Enhances the Antitumor Efficacy of Peripheral Peptide-Based Vaccines Cancer Res., August 15, 2004; 64(16): 5830 - 5838. [Abstract] [Full Text] [PDF]
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Y.-P. Liao, C.-C. Wang, L. H. Butterfield, J. S. Economou, A. Ribas, W. S. Meng, K. S. Iwamoto, and W. H. McBride Ionizing Radiation Affects Human MART-1 Melanoma Antigen Processing and Presentation by Dendritic Cells J. Immunol., August 15, 2004; 173(4): 2462 - 2469. [Abstract] [Full Text] [PDF]
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R. Lande, E. Giacomini, B. Serafini, B. Rosicarelli, G. D. Sebastiani, G. Minisola, U. Tarantino, V. Riccieri, G. Valesini, and E. M. Coccia Characterization and Recruitment of Plasmacytoid Dendritic Cells in Synovial Fluid and Tissue of Patients with Chronic Inflammatory Arthritis J. Immunol., August 15, 2004; 173(4): 2815 - 2824. [Abstract] [Full Text] [PDF]
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M. Franchini, H. Hefti, S. Vollstedt, B. Glanzmann, M. Riesen, M. Ackermann, P. Chaplin, K. Shortman, and M. Suter Dendritic Cells from Mice Neonatally Vaccinated with Modified Vaccinia Virus Ankara Transfer Resistance against Herpes Simplex Virus Type I to Naive One-Week-Old Mice J. Immunol., May 15, 2004; 172(10): 6304 - 6312. [Abstract] [Full Text] [PDF]
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L. Gabriele, P. Borghi, C. Rozera, P. Sestili, M. Andreotti, A. Guarini, E. Montefusco, R. Foa, and F. Belardelli IFN-{alpha} promotes the rapid differentiation of monocytes from patients with chronic myeloid leukemia into activated dendritic cells tuned to undergo full maturation after LPS treatment Blood, February 1, 2004; 103(3): 980 - 987. [Abstract] [Full Text] [PDF]
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T. Nagai, O. Devergne, T. F. Mueller, D. L. Perkins, J. M. van Seventer, and G. A. van Seventer Timing of IFN-{beta} Exposure during Human Dendritic Cell Maturation and Naive Th Cell Stimulation Has Contrasting Effects on Th1 Subset Generation: A Role for IFN-{beta}-Mediated Regulation of IL-12 Family Cytokines and IL-18 in Naive Th Cell Differentiation J. Immunol., November 15, 2003; 171(10): 5233 - 5243. [Abstract] [Full Text] [PDF]
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M. Mohty, A. Vialle-Castellano, J. A. Nunes, D. Isnardon, D. Olive, and B. Gaugler IFN-{alpha} Skews Monocyte Differentiation into Toll-Like Receptor 7-Expressing Dendritic Cells with Potent Functional Activities J. Immunol., October 1, 2003; 171(7): 3385 - 3393. [Abstract] [Full Text] [PDF]
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M. Obuchi, M. Fernandez, and G. N. Barber Development of Recombinant Vesicular Stomatitis Viruses That Exploit Defects in Host Defense To Augment Specific Oncolytic Activity J. Virol., August 15, 2003; 77(16): 8843 - 8856. [Abstract] [Full Text] [PDF]
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F. Moschella, B. Bisikirska, A. Maffei, K. P. Papadopoulos, D. Skerrett, Z. Liu, C. S. Hesdorffer, and P. E. Harris Gene Expression Profiling and Functional Activity of Human Dendritic Cells Induced with IFN-{alpha}-2b: Implications for Cancer Immunotherapy Clin. Cancer Res., June 1, 2003; 9(6): 2022 - 2031. [Abstract] [Full Text] [PDF]
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A. Krug, S. Rothenfusser, S. Selinger, C. Bock, M. Kerkmann, J. Battiany, A. Sarris, T. Giese, D. Speiser, S. Endres, et al. CpG-A Oligonucleotides Induce a Monocyte-Derived Dendritic Cell-Like Phenotype That Preferentially Activates CD8 T Cells J. Immunol., April 1, 2003; 170(7): 3468 - 3477. [Abstract] [Full Text] [PDF]
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V. S. Cull, P. A. Tilbrook, E. J. Bartlett, N. L. Brekalo, and C. M. James Type I interferon differential therapy for erythroleukemia: specificity of STAT activation Blood, April 1, 2003; 101(7): 2727 - 2735. [Abstract] [Full Text] [PDF]
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R. Lande, E. Giacomini, T. Grassi, M. E. Remoli, E. Iona, M. Miettinen, I. Julkunen, and E. M. Coccia IFN-{alpha}{beta} Released by Mycobacterium tuberculosis-Infected Human Dendritic Cells Induces the Expression of CXCL10: Selective Recruitment of NK and Activated T Cells J. Immunol., February 1, 2003; 170(3): 1174 - 1182. [Abstract] [Full Text] [PDF]
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J. L. Miller and E. M. Anders Virus-cell interactions in the induction of type 1 interferon by influenza virus in mouse spleen cells J. Gen. Virol., January 1, 2003; 84(1): 193 - 202. [Abstract] [Full Text] [PDF]
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M. C. Gauzzi, I. Canini, P. Eid, F. Belardelli, and S. Gessani Loss of Type I IFN Receptors and Impaired IFN Responsiveness During Terminal Maturation of Monocyte-Derived Human Dendritic Cells J. Immunol., September 15, 2002; 169(6): 3038 - 3045. [Abstract] [Full Text] [PDF]
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B. D. Brown and D. Lillicrap Dangerous liaisons: the role of "danger" signals in the immune response to gene therapy Blood, July 30, 2002; 100(4): 1133 - 1140. [Abstract] [Full Text] [PDF]
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T. Luft, M. Jefford, P. Luetjens, T. Toy, H. Hochrein, K.-A. Masterman, C. Maliszewski, K. Shortman, J. Cebon, and E. Maraskovsky Functionally distinct dendritic cell (DC) populations induced by physiologic stimuli: prostaglandin E2 regulates the migratory capacity of specific DC subsets Blood, July 30, 2002; 100(4): 1362 - 1372. [Abstract] [Full Text] [PDF]
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K. Abel, M. J. Alegria-Hartman, K. Rothaeusler, M. Marthas, and C. J. Miller The Relationship between Simian Immunodeficiency Virus RNA Levels and the mRNA Levels of Alpha/Beta Interferons (IFN-{alpha}/{beta}) and IFN-{alpha}/{beta}-Inducible Mx in Lymphoid Tissues of Rhesus Macaques during Acute and Chronic Infection J. Virol., July 17, 2002; 76(16): 8433 - 8445. [Abstract] [Full Text] [PDF]
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M. E. Remoli, E. Giacomini, G. Lutfalla, E. Dondi, G. Orefici, A. Battistini, G. Uze, S. Pellegrini, and E. M. Coccia Selective Expression of Type I IFN Genes in Human Dendritic Cells Infected with Mycobacterium tuberculosis J. Immunol., July 1, 2002; 169(1): 366 - 374. [Abstract] [Full Text] [PDF]
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E. Proietti, L. Bracci, S. Puzelli, T. Di Pucchio, P. Sestili, E. De Vincenzi, M. Venditti, I. Capone, I. Seif, E. De Maeyer, et al. Type I IFN as a Natural Adjuvant for a Protective Immune Response: Lessons from the Influenza Vaccine Model J. Immunol., July 1, 2002; 169(1): 375 - 383. [Abstract] [Full Text] [PDF]
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S. Sasaki, R. R. Amara, W.-S. Yeow, P. M. Pitha, and H. L. Robinson Regulation of DNA-Raised Immune Responses by Cotransfected Interferon Regulatory Factors J. Virol., June 5, 2002; 76(13): 6652 - 6659. [Abstract] [Full Text] [PDF]
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M. Montoya, G. Schiavoni, F. Mattei, I. Gresser, F. Belardelli, P. Borrow, and D. F. Tough Type I interferons produced by dendritic cells promote their phenotypic and functional activation Blood, May 1, 2002; 99(9): 3263 - 3271. [Abstract] [Full Text] [PDF]
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E. Padovan, G. C. Spagnoli, M. Ferrantini, and M. Heberer IFN-{alpha}2a induces IP-10/CXCL10 and MIG/CXCL9 production in monocyte-derived dendritic cells and enhances their capacity to attract and stimulate CD8+ effector T cells J. Leukoc. Biol., April 1, 2002; 71(4): 669 - 676. [Abstract] [Full Text] [PDF]
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C. Buelens, E. J. Bartholome, Z. Amraoui, M. Boutriaux, I. Salmon, K. Thielemans, F. Willems, and M. Goldman Interleukin-3 and interferon beta cooperate to induce differentiation of monocytes into dendritic cells with potent helper T-cell stimulatory properties Blood, February 1, 2002; 99(3): 993 - 998. [Abstract] [Full Text] [PDF]
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H. Zheng, J. Dai, D. Stoilova, and Z. Li Cell Surface Targeting of Heat Shock Protein gp96 Induces Dendritic Cell Maturation and Antitumor Immunity J. Immunol., December 15, 2001; 167(12): 6731 - 6735. [Abstract] [Full Text] [PDF]
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H. Donaghy, A. Pozniak, B. Gazzard, N. Qazi, J. Gilmour, F. Gotch, and S. Patterson Loss of blood CD11c+ myeloid and CD11c{-} plasmacytoid dendritic cells in patients with HIV-1 infection correlates with HIV-1 RNA virus load Blood, October 15, 2001; 98(8): 2574 - 2576. [Abstract] [Full Text] [PDF]
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T. Luft, M. Rizkalla, T. Y. Tai, Q. Chen, R. I. MacFarlan, I. D. Davis, E. Maraskovsky, and J. Cebon Exogenous Peptides Presented by Transporter Associated with Antigen Processing (TAP)-Deficient and TAP-Competent Cells: Intracellular Loading and Kinetics of Presentation J. Immunol., September 1, 2001; 167(5): 2529 - 2537. [Abstract] [Full Text] [PDF]
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A. E. Morelli, A. F. Zahorchak, A. T. Larregina, B. L. Colvin, A. J. Logar, T. Takayama, L. D. Falo, and A. W. Thomson Cytokine production by mouse myeloid dendritic cells in relation to differentiation and terminal maturation induced by lipopolysaccharide or CD40 ligation Blood, September 1, 2001; 98(5): 1512 - 1523. [Abstract] [Full Text] [PDF]
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F. Mattei, G. Schiavoni, F. Belardelli, and D. F. Tough IL-15 Is Expressed by Dendritic Cells in Response to Type I IFN, Double-Stranded RNA, or Lipopolysaccharide and Promotes Dendritic Cell Activation J. Immunol., August 1, 2001; 167(3): 1179 - 1187. [Abstract] [Full Text] [PDF]
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E. Giacomini, E. Iona, L. Ferroni, M. Miettinen, L. Fattorini, G. Orefici, I. Julkunen, and E. M. Coccia Infection of Human Macrophages and Dendritic Cells with Mycobacterium tuberculosis Induces a Differential Cytokine Gene Expression That Modulates T Cell Response J. Immunol., June 15, 2001; 166(12): 7033 - 7041. [Abstract] [Full Text] [PDF]
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D. H. Libraty, S. Pichyangkul, C. Ajariyakhajorn, T. P. Endy, and F. A. Ennis Human Dendritic Cells Are Activated by Dengue Virus Infection: Enhancement by Gamma Interferon and Implications for Disease Pathogenesis J. Virol., April 15, 2001; 75(8): 3501 - 3508. [Abstract] [Full Text]
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D. Rea, M. J. E. Havenga, M. van den Assem, R. P. M. Sutmuller, A. Lemckert, R. C. Hoeben, A. Bout, C. J. M. Melief, and R. Offringa Highly Efficient Transduction of Human Monocyte-Derived Dendritic Cells with Subgroup B Fiber-Modified Adenovirus Vectors Enhances Transgene-Encoded Antigen Presentation to Cytotoxic T Cells J. Immunol., April 15, 2001; 166(8): 5236 - 5244. [Abstract] [Full Text] [PDF]
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Y.-M. Huang, M. Kouwenhoven, Y.-P. Jin, R. Press, W.-X. Huang, and H. Link Dendritic cells derived from patients with multiple sclerosis show high CD1a and low CD86 expression Multiple Sclerosis, April 1, 2001; 7(2): 95 - 99. [Abstract] [PDF]
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C. Menetrier-Caux, M. C. Thomachot, L. Alberti, G. Montmain, and J. Y. Blay IL-4 Prevents the Blockade of Dendritic Cell Differentiation Induced by Tumor Cells Cancer Res., April 1, 2001; 61(7): 3096 - 3104. [Abstract] [Full Text]
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T. Ito, R. Amakawa, M. Inaba, S. Ikehara, K. Inaba, and S. Fukuhara Differential Regulation of Human Blood Dendritic Cell Subsets by IFNs J. Immunol., March 1, 2001; 166(5): 2961 - 2969. [Abstract] [Full Text] [PDF]
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M. P. Hardy, C. M. Owczarek, S. Trajanovska, X. Liu, I. Kola, and P. J. Hertzog The soluble murine type I interferon receptor Ifnar-2 is present in serum, is independently regulated, and has both agonistic and antagonistic properties Blood, January 15, 2001; 97(2): 473 - 482. [Abstract] [Full Text] [PDF]
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E. Riedl, J. Stockl, O. Majdic, C. Scheinecker, W. Knapp, and H. Strobl Ligation of E-cadherin on in vitro-generated immature Langerhans-type dendritic cells inhibits their maturation Blood, December 15, 2000; 96(13): 4276 - 4284. [Abstract] [Full Text] [PDF]
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R. Ignatius, M. Marovich, E. Mehlhop, L. Villamide, K. Mahnke, W. I. Cox, F. Isdell, S. S. Frankel, J. R. Mascola, R. M. Steinman, et al. Canarypox Virus-Induced Maturation of Dendritic Cells Is Mediated by Apoptotic Cell Death and Tumor Necrosis Factor Alpha Secretion J. Virol., December 1, 2000; 74(23): 11329 - 11338. [Abstract] [Full Text]
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) and 28 days (
) using the same allogeneic responder cells
for both time points. DC were cultured in GM-CSF, TNF-
), (n
= 6), p < 0.05. B, Allostimulatory
function of DC sorted on day 18. Culture was split on day 14 and either
continued in GM-CSF, TNF-