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CUTTING EDGE |
*
Department of Molecular Biology, Princeton University, Princeton, NJ 08544;
Institut National de la Santé et de la Recherche Médicale U25, Hopital Necker, Paris, France; and
Pharmaceutical Research Laboratory, Kirin Brewery Co., Ltd, Gunma, Japan
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Abstract |
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 Top Abstract IntroductionMaterials and MethodsResults and DiscussionReferences |
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-Galactosylceramide (-GalCer) is a glycolipid with potent
antitumor properties that binds to CD1d molecules and activates mouse
V14 and human V24 NKT cells. Surprisingly, we found that, as
early as 90 min after -GalCer injection in vivo, NK cells also
displayed considerable signs of activation, including IFN-
production and CD69 induction. NK activation was not observed in RAG-
or CD1-deficient mice, and it was decreased by pretreatment with
anti-IFN- Abs, suggesting that, despite its rapid induction, it
was a secondary event that depended on IFN- release by NKT cells. At
later time points, B cells and CD8 T cells also began to express CD69.
These findings identify a high-speed communication network between the
innate and adaptive immune systems in vivo that is initiated upon NKT
cell activation. They also suggest that the antitumor effects of
-GalCer result from the sequential recruitment of distinct
innate and adaptive effector lymphocytes. |
Introduction |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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for
NK cells, and IFN- and IL-4 for NKT cells. In addition, they both
constitute relatively large populations, on the order of 1–30% of
total lymphocytes in different tissues (reviewed in ref
(1, 2, 3).
NKT cells use semi-invariant TCRs (4) to recognize
glycolipids, such as -galactosylceramide
(-GalCer)3
presented by CD1d molecules (5). In addition, cytokines
such as IL-12 can stimulate both NK cells (6) and NKT
cells (7, 8) to release IFN- and express natural
cytotoxicity. The rapid activation of both these populations is
characteristic of innate immunity and probably serves two purposes: to
provide a first line of defense against pathogens and to orient the
adaptive immune response into the appropriate effector pathway
according to the nature of the pathogen.
NK and NKT cells have been implicated in a wide spectrum of conditions.
NK cells play a role in viral infections, especially of the Herpes
virus type, and can also function against intracellular pathogens and
tumors. NKT cells exert regulatory functions, most likely through their
capacity to promptly release large amounts of IL-4 to orient responses
in a Th2 direction (9, 10). NKT cells can prevent type 1
diabetes in the nonobese diabetic (NOD) mouse (11, 12) and
possibly also in humans (13), and participate in a variety
of responses against infections (14, 15). However, recent
studies have generated some confusion with regard to the respective
roles of NK and NKT cells. Effector functions against tumors,
originally attributed to NK cells, have been ascribed to NKT cells
(8, 16), and conversely some immunoregulatory functions,
such as those exerted upon experimental autoimmune encephalomyelitis
(17) or eosinophilic airway disease
(18), have been associated with classical NK cells rather
than with NKT cells. These reports led us to consider the possibility
that NK and NKT cells might be functionally linked in vivo, the
activation of one leading to the activation of the other, thus
explaining the ambiguity in the definition and apportioning of their
roles. To test this idea, we took advantage of the ability of
-GalCer, a synthetic glycolipid
(2S,3S,4R)-1-O-(-D-galactopyranosyl)-2-(N-hexacosanoylamino)-1,3,4,-octadecanetriol)
(KRN 7000) to stimulate essentially all mouse V14 and human V24
NKT cells (5, 19, 20). -GalCer is chemically and
functionally analogous to natural glycolipids that were first purified
from marine sponges on the basis of their antitumor properties against
the mouse B16 melanoma (21, 22, 23). Our experiments indicate
that NKT cells can transactivate NK cells at a surprisingly high speed
upon stimulation with -GalCer in vivo. Furthermore, the network of
activation initiated by NKT cells extends, with some delay, to B cells
and T cells as well.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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Six- to 12-wk-old C57BL/6J (B6) mice, raised and maintained
under strict specific pathogen-free conditions, were used throughout
these experiments. B6.RAG-/- and B6.TCR
C-/- mice were purchased from The Jackson
Laboratories (Bar Harbor, ME). B6.CD1-/- mice
were generated in our own laboratory from a targeted embryonic stem
cell of 129 origin (S.-H. Park and A. Bendelac, manuscript in
preparation) and used at the seventh backcross generation onto
B6.
Flow cytometry
For intracellular detection of IFN- in NK cells, spleen cells
were first surface-stained with PK136-FITC or DX5-FITC and CD3-Cychrome
or CD5-Cychrome (all from PharMingen, San Diego, CA) at 4°C for 20
mn, then fixed for 5 min in PBS with 4% paraformaldehyde and
permeabilized for 30 min in PBS containing 0.1% saponin and 5%
skimmed milk before staining for 30 min with anti-IFN--PE
(XMG1.2; PharMingen) diluted in PBS-saponin-milk, as described
(24). For studies on CD69 induction, B220-FITC, CD8-PE,
CD4-APC, and CD69-biotin were from PharMingen, and
streptavidin-Tricolor was from Caltag (San Francisco, CA). Cell were
analyzed for fluorescence using a FACScan, FACScalibur or FACS Vantage
and the CellQuest software (Becton Dickinson, San Jose, CA).
In vivo activation of NKT cells
Mice were injected i.v. with 10 µg of -GalCer and their
spleen cells collected at different time points, from 90 min to 6
h after injection. -GalCer was diluted in PBS from a 220 µg/ml
stock solution in 0.5% polysorbate solvent. Controls were injected
with a corresponding dose of solvent. For in vivo blocking of
cytokines, mice were injected i.p. with 1 mg of purified Ab against
IL-4 (11B11), or IFN- (RA4-6A2 or XMG1.2) for 16–24 h before the
injection of -GalCer. The use of RA4-6A2 in some experiments of in
vivo IFN- blocking was to avoid potential interferences with
intracellular staining of IFN- with XMG1.2, as these mAbs do not
compete for binding IFN-.
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Results and Discussion |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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-GalCer injection rapidly activates NK cells to produce IFN-
in vivo
In the experiment shown in Fig. 1
,
mice were injected with 10 µg of -GalCer and killed after 1.5, 3,
or 6 h. The spleen cells were immediately incubated at 4°C with
mAbs specific for cell surface receptors, then processed for
intracellular staining by fixation/permeabilization followed by
incubation with anti-IFN- mAb. By using a highly fluorescent
PE-conjugated anti-IFN- mAb, we were able to detect IFN- in
the cytoplasm of activated cells directly ex vivo, without prior
exposure to brefeldin A in vitro, as is usually required for the
detection of intracellular cytokines (24). Thus, the
results described below reflect purely in vivo events.
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as early as 1.5 h following -GalCer injection (Fig. 1
, A and B). The levels continued to rise until the
6 h time point, where a large fraction of NK cells, ranging from
30 to 50% in different experiments, were found to produce high levels
of IFN-. The IFN- staining profile was often bimodal, indicating
that only a fraction of NK cells were receptive or were receiving the
activation signals.
NKT cells could not be satisfactorily resolved in these experiments for
technical reasons: they express levels of NK1.1 that are 2–3 times
lower than NK cells, and the fixation/permeabilization technique that
allows for intracytoplasmic staining of cytokines significantly reduces
the level of NK1.1 staining, thus preventing clear-cut resolution of
these NK1.1low T cells. In addition, although
cells in the CD3+NK1.1low
double-positive area of the FACS dot plots were found to produce
IFN- as well as IL-4 (data not shown), this region contains
artefactual dots that preclude a rigorous analysis. This is
particularly evident in the RAG-deficient mice (see Fig. 1A,
lower left panel), which do not contain CD3-positive cells
yet display some CD3+NK1.1+
double positive dots that result in part from the
fixation/permeabilization procedure. On the other hand, we eliminated
the possibility that the CD3-negative NK1.1-positive, IFN--producing
cells were NKT cells that had down-modulated their TCR because we
obtained identical results with other staining combinations using
anti-CD5, which is positive on NKT cells and negative on NK cells,
and DX5, which is positive on NK cells and negative on NKT cells
(25) (data not shown). Furthermore, IFN- producing
cells with the CD3-negative NK1.1-positive surface phenotype were also
negative for intracellular anti-CD3
staining (data not
shown).
In vivo activation of NK cells by -GalCer requires a functional
CD1/NKT pathway
RAG-deficient mice have a functional NK cell compartment and
normally express CD1, the -GalCer presenting molecule. However,
their NK cells did not produce IFN- after the injection of
-GalCer (Fig. 1A). A similar result was obtained with TCR
C-deficient mice (data not shown). Thus, despite its very high
speed, NK cell activation appears to be a secondary event that requires
and follows the prior activation of another cell type, likely to be the
NKT cell. Indeed, in CD1-deficient mice, which selectively lack NKT
cells, NK cells failed to produce IFN- (Fig. 1C). This
defective NK cell activation was not due to some intrinsic NK cell
defect, because NK cells of CD1-deficient mice could be normally
activated in vivo as well as in vitro by other stimuli, such as
poly(I:C), an inducer of YAC-1 cytotoxicity, and the combination of
ionomycin and PMA, a potent inducer of IFN- secretion (data not
shown). Altogether, these results indicate that NK cells are
transactivated very rapidly as a consequence of -GalCer-induced
activation of NKT cells.
Widespread induction of CD69 in vivo by injection of -GalCer
NK cells, which constitutively express low levels of CD69, an
early activation marker, started to up-regulate CD69 within 1.5 h
of -GalCer injection, reaching peak levels at 3 h on >50% of
the cells (Fig. 2). This induction of
CD69, was abolished, as expected, in the CD1-deficient mice.
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). CD1-deficient mice
(Fig. 2) and TCR C-deficient mice (data not shown) failed to
up-regulate CD69 on B cells, indicating again the need for prior
activation of NKT cells. In addition, some induction of CD69 was also
observed on CD8 cells and, to a lesser degree, on CD4 cells (Fig. 2). Thus, the lymphoid populations that seem most affected by the activation of NKT cells are, in chronological order, the NK cells and the B and CD8 cells.
Nature of the cross-talk between NKT and NK cells
The very high speed of the transactivation of a large subset of NK
cells after -GalCer-mediated activation of NKT cells suggested that
NK cells might directly respond to the cytokines that are immediately
released by activated NKT cells. To test this hypothesis, mice received
1 mg of neutralizing Abs against IFN- or IL-4, two prominent
cytokines released by NKT cells, 16–24 h before the injection of
-GalCer. Fig. 3 shows that there was a
substantial, though not complete (35% on average) reduction of
intracellular IFN- after in vivo blocking with anti-IFN-, but
not with anti-IL-4 Abs. A similar pattern of partial inhibition of
CD69 induction was observed after anti-IFN- treatment and in
IFN- knockout (KO) mice (data not shown). Thus, the communication
between the two NK subsets involves IFN-, but other factors, such as
additional cytokines and/or surface receptors, may also be required to
achieve full activation.
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Because the antitumor effect of -GalCer was absent in
J281-deficient mice (16) that lack NKT cells, it was
suggested that activated NKT cells might directly kill tumor cells.
However, and in accordance with previous reports that
-GalCer-injected tumor-bearing mice had increased levels of natural
cytotoxicity mediated by "classical" NK cells (26, 27), our studies now reveal a more complex scenario involving
other potential antitumor effectors such as NK cells, as well as CD8 T
cells and B cells. Each of these has the potential to contribute to
tumor rejection.
In conclusion, we show that in vivo engagement of NKT cells by their glycolipid ligand rapidly induces a cascade of cellular activation that involves elements of innate and adaptive immunity and may have far reaching consequences not only on the speed and strength but also on the type of subsequent immune responses, in particular those directed against tumor cells.
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Acknowledgments |
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Footnotes |
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2 Address correspondence and reprint requests to Dr. Claude Carnaud, Institut National de la Santé et de la Recherche Médicale U25, Hôpital Necker, 161 Rue de Sèvres, Paris, 75743 France. E-mail address:
3 Abbreviation used in this paper: -GalCer, -galactosylceramide.
Received for publication August 2, 1999. Accepted for publication September 3, 1999.
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References |
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TopAbstractIntroductionMaterials and MethodsResults and DiscussionReferences |
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chain is used by a unique subset of MHC class I-specific CD4+ and CD4-8- T cells in mice and humans. J. Exp. Med. 180:1097.14 NKT cells by glycosylceramides. Science 278:1626.ß T cells activated by IL-12 as a major effector in inhibition of experimental tumor metastasis. J. Immunol. 156:3366.[Abstract]
14 NKT cells in IL-12-mediated rejection of tumors. Science 278:1623./ß-T cell receptor (TCR)+CD4-CD8- (NKT) thymocytes prevent insulin-dependent diabetes mellitus in nonobese diabetic (NOD)/Lt mice by the influence of interleukin (IL)-4 and/or IL-10. J. Exp. Med. 187:1047.14-J281 transgenic nonobese diabetic mice against diabetes. J. Exp. Med. 188:1831.24JQ T cells in type I diabetes. Nature 391:177.[Medline]
14 NKT cells. Proc. Natl. Acad. Sci. USA 95:5690.-galactosylceramide by natural killer T cells is highly conserved through mammalian evolution. J. Exp. Med. 188:1521.-galactosylceramides against B16-bearing mice. J. Med. Chem. 38:2176.[Medline]
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M. J. Raftery, F. Winau, S. H. E. Kaufmann, U. E. Schaible, and G. Schonrich CD1 Antigen Presentation by Human Dendritic Cells as a Target for Herpes Simplex Virus Immune Evasion J. Immunol., November 1, 2006; 177(9): 6207 - 6214. [Abstract] [Full Text] [PDF]
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 S. Motohashi, A. Ishikawa, E. Ishikawa, M. Otsuji, T. Iizasa, H. Hanaoka, N. Shimizu, S. Horiguchi, Y. Okamoto, S.-i. Fujii, et al. A Phase I Study of In vitro Expanded Natural Killer T Cells in Patients with Advanced and Recurrent Non-Small Cell Lung Cancer Clin. Cancer Res., October 15, 2006; 12(20): 6079 - 6086. [Abstract] [Full Text] [PDF]
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R. R. Brutkiewicz CD1d Ligands: The Good, the Bad, and the Ugly J. Immunol., July 15, 2006; 177(2): 769 - 775. [Abstract] [Full Text] [PDF]
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D. H. Chang, N. Liu, V. Klimek, H. Hassoun, A. Mazumder, S. D. Nimer, S. Jagannath, and M. V. Dhodapkar Enhancement of ligand-dependent activation of human natural killer T cells by lenalidomide: therapeutic implications Blood, July 15, 2006; 108(2): 618 - 621. [Abstract] [Full Text] [PDF]
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J. Larkin, G. J. Renukaradhya, V. Sriram, W. Du, J. Gervay-Hague, and R. R. Brutkiewicz CD44 Differentially Activates Mouse NK T Cells and Conventional T Cells J. Immunol., July 1, 2006; 177(1): 268 - 279. [Abstract] [Full Text] [PDF]
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 J. E. Boyson, N. Nagarkatti, L. Nizam, M. A. Exley, and J. L. Strominger Gestation stage-dependent mechanisms of invariant natural killer T cell-mediated pregnancy loss PNAS, March 21, 2006; 103(12): 4580 - 4585. [Abstract] [Full Text] [PDF]
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T. Mallevaey, J. P. Zanetta, C. Faveeuw, J. Fontaine, E. Maes, F. Platt, M. Capron, M. L. de-Moraes, and F. Trottein Activation of Invariant NKT Cells by the Helminth Parasite Schistosoma mansoni J. Immunol., February 15, 2006; 176(4): 2476 - 2485. [Abstract] [Full Text] [PDF]
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M. I. Zimmer, A. Colmone, K. Felio, H. Xu, A. Ma, and C.-R. Wang A Cell-Type Specific CD1d Expression Program Modulates Invariant NKT Cell Development and Function J. Immunol., February 1, 2006; 176(3): 1421 - 1430. [Abstract] [Full Text] [PDF]
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S. Oki, C. Tomi, T. Yamamura, and S. Miyake Preferential Th2 polarization by OCH is supported by incompetent NKT cell induction of CD40L and following production of inflammatory cytokines by bystander cells in vivo Int. Immunol., December 1, 2005; 17(12): 1619 - 1629. [Abstract] [Full Text] [PDF]
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M. S. Vincent, X. Xiong, E. P. Grant, W. Peng, and M. B. Brenner CD1a-, b-, and c-Restricted TCRs Recognize Both Self and Foreign Antigens J. Immunol., November 15, 2005; 175(10): 6344 - 6351. [Abstract] [Full Text] [PDF]
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M. Svensson, S. Zubairi, A. Maroof, F. Kazi, M. Taniguchi, and P. M. Kaye Invariant NKT Cells Are Essential for the Regulation of Hepatic CXCL10 Gene Expression during Leishmania donovani Infection Infect. Immun., November 1, 2005; 73(11): 7541 - 7547. [Abstract] [Full Text] [PDF]
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S. Patterson, I. Kotsianidis, A. Almeida, M. Politou, A. Rahemtulla, B. Matthew, R. R. Schmidt, V. Cerundolo, I. A. G. Roberts, and A. Karadimitris Human Invariant NKT Cells Are Required for Effective In Vitro Alloresponses J. Immunol., October 15, 2005; 175(8): 5087 - 5094. [Abstract] [Full Text] [PDF]
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A. P. Uldrich, N. Y. Crowe, K. Kyparissoudis, D. G. Pellicci, Y. Zhan, A. M. Lew, P. Bouillet, A. Strasser, M. J. Smyth, and D. I. Godfrey NKT Cell Stimulation with Glycolipid Antigen In Vivo: Costimulation-Dependent Expansion, Bim-Dependent Contraction, and Hyporesponsiveness to Further Antigenic Challenge J. Immunol., September 1, 2005; 175(5): 3092 - 3101. [Abstract] [Full Text] [PDF]
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S. Uehara, C. M. Chase, W. H. Kitchens, H. S. Rose, R. B. Colvin, P. S. Russell, and J. C. Madsen NK Cells Can Trigger Allograft Vasculopathy: The Role of Hybrid Resistance in Solid Organ Allografts J. Immunol., September 1, 2005; 175(5): 3424 - 3430. [Abstract] [Full Text] [PDF]
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T. Osada, M. A. Morse, H. K. Lyerly, and T. M. Clay Ex vivo expanded human CD4+ regulatory NKT cells suppress expansion of tumor antigen-specific CTLs Int. Immunol., September 1, 2005; 17(9): 1143 - 1155. [Abstract] [Full Text] [PDF]
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S. C. Yue, A. Shaulov, R. Wang, S. P. Balk, and M. A. Exley CD1d ligation on human monocytes directly signals rapid NF-{kappa}B activation and production of bioactive IL-12 PNAS, August 16, 2005; 102(33): 11811 - 11816. [Abstract] [Full Text] [PDF]
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M. Biburger and G. Tiegs {alpha}-Galactosylceramide-Induced Liver Injury in Mice Is Mediated by TNF-{alpha} but Independent of Kupffer Cells J. Immunol., August 1, 2005; 175(3): 1540 - 1550. [Abstract] [Full Text] [PDF]
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C. Forestier, A. Molano, J. S. Im, Y. Dutronc, B. Diamond, A. Davidson, P. A. Illarionov, G. S. Besra, and S. A. Porcelli Expansion and Hyperactivity of CD1d-Restricted NKT Cells during the Progression of Systemic Lupus Erythematosus in (New Zealand Black x New Zealand White)F1 Mice J. Immunol., July 15, 2005; 175(2): 763 - 770. [Abstract] [Full Text] [PDF]
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Y. Geng, P. Laslo, K. Barton, and C.-R. Wang Transcriptional Regulation of CD1D1 by Ets Family Transcription Factors J. Immunol., July 15, 2005; 175(2): 1022 - 1029. [Abstract] [Full Text] [PDF]
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T. Ranson, S. Bregenholt, A. Lehuen, O. Gaillot, M. C. Leite-de-Moraes, A. Herbelin, P. Berche, and J. P. Di Santo Invariant V{alpha}14+ NKT Cells Participate in the Early Response to Enteric Listeria monocytogenes Infection J. Immunol., July 15, 2005; 175(2): 1137 - 1144. [Abstract] [Full Text] [PDF]
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T. Ota, K. Takeda, H. Akiba, Y. Hayakawa, K. Ogasawara, Y. Ikarashi, S. Miyake, H. Wakasugi, T. Yamamura, M. Kronenberg, et al. IFN-{gamma}-mediated negative feedback regulation of NKT-cell function by CD94/NKG2 Blood, July 1, 2005; 106(1): 184 - 192. [Abstract] [Full Text] [PDF]
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M. J. Smyth, M. E. Wallace, S. L. Nutt, H. Yagita, D. I. Godfrey, and Y. Hayakawa Sequential activation of NKT cells and NK cells provides effective innate immunotherapy of cancer J. Exp. Med., June 20, 2005; 201(12): 1973 - 1985. [Abstract] [Full Text] [PDF]
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D. H. Chang, K. Osman, J. Connolly, A. Kukreja, J. Krasovsky, M. Pack, A. Hutchinson, M. Geller, N. Liu, R. Annable, et al. Sustained expansion of NKT cells and antigen-specific T cells after injection of {alpha}-galactosyl-ceramide loaded mature dendritic cells in cancer patients J. Exp. Med., May 2, 2005; 201(9): 1503 - 1517. [Abstract] [Full Text] [PDF]
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 P. A. VanderLaan and C. A. Reardon Thematic review series: The Immune System and Atherogenesis. The unusual suspects:an overview of the minor leukocyte populations in atherosclerosis J. Lipid Res., May 1, 2005; 46(5): 829 - 838. [Abstract] [Full Text] [PDF]
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M. S. Duthie and S. J. Kahn NK cell activation and protection occur independently of natural killer T cells during Trypanosoma cruzi infection Int. Immunol., May 1, 2005; 17(5): 607 - 613. [Abstract] [Full Text] [PDF]
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J. S. Bezbradica, A. K. Stanic, N. Matsuki, H. Bour-Jordan, J. A. Bluestone, J. W. Thomas, D. Unutmaz, L. Van Kaer, and S. Joyce Distinct Roles of Dendritic Cells and B Cells in Va14Ja18 Natural T Cell Activation In Vivo J. Immunol., April 15, 2005; 174(8): 4696 - 4705. [Abstract] [Full Text] [PDF]
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D. S. Hansen, K. J. Evans, M. C. D'Ombrain, N. J. Bernard, A. C. Sexton, L. Buckingham, A. A. Scalzo, and L. Schofield The Natural Killer Complex Regulates Severe Malarial Pathogenesis and Influences Acquired Immune Responses to Plasmodium berghei ANKA Infect. Immun., April 1, 2005; 73(4): 2288 - 2297. [Abstract] [Full Text] [PDF]
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J. D. Wesley, S. H. Robbins, S. Sidobre, M. Kronenberg, S. Terrizzi, and L. Brossay Cutting Edge: IFN-{gamma} Signaling to Macrophages Is Required for Optimal V{alpha}14i NK T/NK Cell Cross-Talk J. Immunol., April 1, 2005; 174(7): 3864 - 3868. [Abstract] [Full Text] [PDF]
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B. Chung, A. Aoukaty, J. Dutz, C. Terhorst, and R. Tan Cutting Edge: Signaling Lymphocytic Activation Molecule-Associated Protein Controls NKT Cell Functions J. Immunol., March 15, 2005; 174(6): 3153 - 3157. [Abstract] [Full Text] [PDF]
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K. O. A. Yu, J. S. Im, A. Molano, Y. Dutronc, P. A. Illarionov, C. Forestier, N. Fujiwara, I. Arias, S. Miyake, T. Yamamura, et al. Modulation of CD1d-restricted NKT cell responses by using N-acyl variants of {alpha}-galactosylceramides PNAS, March 1, 2005; 102(9): 3383 - 3388. [Abstract] [Full Text] [PDF]
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 A. M. Aslanian, H. A. Chapman, and I. F. Charo Transient Role for CD1d-Restricted Natural Killer T Cells in the Formation of Atherosclerotic Lesions Arterioscler Thromb Vasc Biol, March 1, 2005; 25(3): 628 - 632. [Abstract] [Full Text] [PDF]
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A. Ishikawa, S. Motohashi, E. Ishikawa, H. Fuchida, K. Higashino, M. Otsuji, T. Iizasa, T. Nakayama, M. Taniguchi, and T. Fujisawa A Phase I Study of {alpha}-Galactosylceramide (KRN7000)-Pulsed Dendritic Cells in Patients with Advanced and Recurrent Non-Small Cell Lung Cancer Clin. Cancer Res., March 1, 2005; 11(5): 1910 - 1917. [Abstract] [Full Text] [PDF]
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S. Korten, R. J. Anderson, C. M. Hannan, E. G. Sheu, R. Sinden, S. Gadola, M. Taniguchi, and A. V. S. Hill Invariant V{alpha}14 Chain NKT Cells Promote Plasmodium berghei Circumsporozoite Protein-Specific Gamma Interferon- and Tumor Necrosis Factor Alpha-Producing CD8+ T Cells in the Liver after Poxvirus Vaccination of Mice Infect. Immun., February 1, 2005; 73(2): 849 - 858. [Abstract] [Full Text] [PDF]
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J. Schmieg, G. Yang, R. W. Franck, N. Van Rooijen, and M. Tsuji Glycolipid presentation to natural killer T cells differs in an organ-dependent fashion PNAS, January 25, 2005; 102(4): 1127 - 1132. [Abstract] [Full Text] [PDF]
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J. Loh, D. T. Chu, A. K. O'Guin, W. M. Yokoyama, and H. W. Virgin IV Natural Killer Cells Utilize both Perforin and Gamma Interferon To Regulate Murine Cytomegalovirus Infection in the Spleen and Liver J. Virol., January 1, 2005; 79(1): 661 - 667. [Abstract] [Full Text] [PDF]
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T. Crough, M. Nieda, and A. J. Nicol Granulocyte Colony-Stimulating Factor Modulates {alpha}-Galactosylceramide-Responsive Human V{alpha}24+V{beta}11+ NKT Cells J. Immunol., October 15, 2004; 173(8): 4960 - 4966. [Abstract] [Full Text] [PDF]
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A. Ahmad and F. Alvarez Role of NK and NKT cells in the immunopathogenesis of HCV-induced hepatitis J. Leukoc. Biol., October 1, 2004; 76(4): 743 - 759. [Abstract] [Full Text] [PDF]
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V. V. Parekh, A. K. Singh, M. T. Wilson, D. Olivares-Villagomez, J. S. Bezbradica, H. Inazawa, H. Ehara, T. Sakai, I. Serizawa, L. Wu, et al. Quantitative and Qualitative Differences in the In Vivo Response of NKT Cells to Distinct {alpha}- and {beta}-Anomeric Glycolipids J. Immunol., September 15, 2004; 173(6): 3693 - 3706. [Abstract] [Full Text] [PDF]
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J. E. Gumperz CD1d-restricted "NKT" cells and myeloid IL-12 production: an immunological crossroads leading to promotion or suppression of effective anti-tumor immune responses? J. Leukoc. Biol., August 1, 2004; 76(2): 307 - 313. [Abstract] [Full Text] [PDF]
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E. Durante-Mangoni, R. Wang, A. Shaulov, Q. He, I. Nasser, N. Afdhal, M. J. Koziel, and M. A. Exley Hepatic CD1d Expression in Hepatitis C Virus Infection and Recognition by Resident Proinflammatory CD1d-Reactive T Cells J. Immunol., August 1, 2004; 173(3): 2159 - 2166. [Abstract] [Full Text] [PDF]
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S. H. Robbins, M. S. Tessmer, T. Mikayama, and L. Brossay Expansion and Contraction of the NK Cell Compartment in Response to Murine Cytomegalovirus Infection J. Immunol., July 1, 2004; 173(1): 259 - 266. [Abstract] [Full Text] [PDF]
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T. Saito, A. Okumura, H. Watanabe, M. Asano, A. Ishida-Okawara, J. Sakagami, K. Sudo, Y. Hatano-Yokoe, J. S. Bezbradica, S. Joyce, et al. Increase in Hepatic NKT Cells in Leukocyte Cell-Derived Chemotaxin 2-Deficient Mice Contributes to Severe Concanavalin A-Induced Hepatitis J. Immunol., July 1, 2004; 173(1): 579 - 585. [Abstract] [Full Text] [PDF]
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L.-P. Ho, B. C. Urban, L. Jones, G. S. Ogg, and A. J. McMichael CD4-CD8{alpha}{alpha} Subset of CD1d-Restricted NKT Cells Controls T Cell Expansion J. Immunol., June 15, 2004; 172(12): 7350 - 7358. [Abstract] [Full Text] [PDF]
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R. Nakagawa, T. Inui, I. Nagafune, Y. Tazunoki, K. Motoki, A. Yamauchi, M. Hirashima, Y. Habu, H. Nakashima, and S. Seki Essential Role of Bystander Cytotoxic CD122+CD8+ T Cells for the Antitumor Immunity Induced in the Liver of Mice by {alpha}-Galactosylceramide J. Immunol., June 1, 2004; 172(11): 6550 - 6557. [Abstract] [Full Text] [PDF]
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P. Gadue, L. Yin, S. Jain, and P. L. Stein Restoration of NK T Cell Development in fyn-Mutant Mice by a TCR Reveals a Requirement for Fyn During Early NK T Cell Ontogeny J. Immunol., May 15, 2004; 172(10): 6093 - 6100. [Abstract] [Full Text] [PDF]
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K. A. Muhlen, J. Schumann, F. Wittke, S. Stenger, N. van Rooijen, L. van Kaer, and G. Tiegs NK Cells, but Not NKT Cells, Are Involved in Pseudomonas aeruginosa Exotoxin A-Induced Hepatotoxicity in Mice J. Immunol., March 1, 2004; 172(5): 3034 - 3041. [Abstract] [Full Text] [PDF]
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K. Schroder, P. J. Hertzog, T. Ravasi, and D. A. Hume Interferon-{gamma}: an overview of signals, mechanisms and functions J. Leukoc. Biol., February 1, 2004; 75(2): 163 - 189. [Abstract] [Full Text] [PDF]
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I-F. Lee, H. Qin, J. Trudeau, J. Dutz, and R. Tan Regulation of Autoimmune Diabetes by Complete Freund's Adjuvant Is Mediated by NK Cells J. Immunol., January 15, 2004; 172(2): 937 - 942. [Abstract] [Full Text] [PDF]
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M. Nieda, M. Okai, A. Tazbirkova, H. Lin, A. Yamaura, K. Ide, R. Abraham, T. Juji, D. J. Macfarlane, and A. J. Nicol Therapeutic activation of V{alpha}24+V{beta}11+ NKT cells in human subjects results in highly coordinated secondary activation of acquired and innate immunity Blood, January 15, 2004; 103(2): 383 - 389. [Abstract] [Full Text] [PDF]
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J. Schmieg, G. Yang, R. W. Franck, and M. Tsuji Superior Protection against Malaria and Melanoma Metastases by a C-glycoside Analogue of the Natural Killer T Cell Ligand {alpha}-Galactosylceramide J. Exp. Med., December 1, 2003; 198(11): 1631 - 1641. [Abstract] [Full Text] [PDF]
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I. F. Hermans, J. D. Silk, U. Gileadi, M. Salio, B. Mathew, G. Ritter, R. Schmidt, A. L. Harris, L. Old, and V. Cerundolo NKT Cells Enhance CD4+ and CD8+ T Cell Responses to Soluble Antigen In Vivo through Direct Interaction with Dendritic Cells J. Immunol., November 15, 2003; 171(10): 5140 - 5147. [Abstract] [Full Text] [PDF]
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A. K. Stanic, R. Shashidharamurthy, J. S. Bezbradica, N. Matsuki, Y. Yoshimura, S. Miyake, E. Y. Choi, T. D. Schell, L. Van Kaer, S. S. Tevethia, et al. Another View of T Cell Antigen Recognition: Cooperative Engagement of Glycolipid Antigens by Va14Ja18 Natural TCR J. Immunol., November 1, 2003; 171(9): 4539 - 4551. [Abstract] [Full Text] [PDF]
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M. Emoto, M. Miyamoto, Y. Emoto, I. Yoshizawa, V. Brinkmann, N. van Rooijen, and S. H. E. Kaufmann Highly Biased Type 1 Immune Responses in Mice Deficient in LFA-1 in Listeria monocytogenes Infection Are Caused by Elevated IL-12 Production by Granulocytes J. Immunol., October 15, 2003; 171(8): 3970 - 3976. [Abstract] [Full Text] [PDF]
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H. Xu, T. Chun, A. Colmone, H. Nguyen, and C.-R. Wang Expression of CD1d Under the Control of a MHC Class Ia Promoter Skews the Development of NKT Cells, But Not CD8+ T Cells J. Immunol., October 15, 2003; 171(8): 4105 - 4112. [Abstract] [Full Text] [PDF]
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M. Skold and S. M. Behar Role of CD1d-Restricted NKT Cells in Microbial Immunity Infect. Immun., October 1, 2003; 71(10): 5447 - 5455. [Full Text] [PDF]
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M. T. Wilson, C. Johansson, D. Olivares-Villagomez, A. K. Singh, A. K. Stanic, C.-R. Wang, S. Joyce, M. J. Wick, and L. Van Kaer The response of natural killer T cells to glycolipid antigens is characterized by surface receptor down-modulation and expansion PNAS, September 16, 2003; 100(19): 10913 - 10918. [Abstract] [Full Text] [PDF]
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L. M. Esteban, T. Tsoutsman, M. A. Jordan, D. Roach, L. D. Poulton, A. Brooks, O. V. Naidenko, S. Sidobre, D. I. Godfrey, and A. G. Baxter Genetic Control of NKT Cell Numbers Maps to Major Diabetes and Lupus Loci J. Immunol., September 15, 2003; 171(6): 2873 - 2878. [Abstract] [Full Text] [PDF]
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C. N. Baxevanis, A. D. Gritzapis, and M. Papamichail In Vivo Antitumor Activity of NKT Cells Activated by the Combination of IL-12 and IL-18 J. Immunol., September 15, 2003; 171(6): 2953 - 2959. [Abstract] [Full Text] [PDF]
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T. A. Moore, M. L. Perry, A. G. Getsoian, C. L. Monteleon, A. L. Cogen, and T. J. Standiford Increased Mortality and Dysregulated Cytokine Production in Tumor Necrosis Factor Receptor 1-Deficient Mice following Systemic Klebsiella pneumoniae Infection Infect. Immun., September 1, 2003; 71(9): 4891 - 4900. [Abstract] [Full Text] [PDF]
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Y. Hayakawa, S. Rovero, G. Forni, and M. J. Smyth {alpha}-Galactosylceramide (KRN7000) suppression of chemical- and oncogene-dependent carcinogenesis PNAS, August 5, 2003; 100(16): 9464 - 9469. [Abstract] [Full Text] [PDF]
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S. Gillessen, Y. N. Naumov, E. E. S. Nieuwenhuis, M. A. Exley, F. S. Lee, N. Mach, A. D. Luster, R. S. Blumberg, M. Taniguchi, S. P. Balk, et al. CD1d-restricted T cells regulate dendritic cell function and antitumor immunity in a granulocyte-macrophage colony-stimulating factor-dependent fashion PNAS, July 22, 2003; 100(15): 8874 - 8879. [Abstract] [Full Text] [PDF]
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S.-i. Fujii, K. Shimizu, C. Smith, L. Bonifaz, and R. M. Steinman Activation of Natural Killer T Cells by {alpha}-Galactosylceramide Rapidly Induces the Full Maturation of Dendritic Cells In Vivo and Thereby Acts as an Adjuvant for Combined CD4 and CD8 T Cell Immunity to a Coadministered Protein J. Exp. Med., July 21, 2003; 198(2): 267 - 279. [Abstract] [Full Text] [PDF]
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