| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
í Plach
*
Medical Policlinic, University of Munich, Munich, Germany;
Institute for Animal Physiology, University of Munich, Munich, Germany;
Serono Pharmaceutical Research Institute, Geneva, Switzerland; and
Institute of Molecular Genetics, Czech Academy of Sciences, Prague, Czech Republic
 |
Abstract |
|---|
 Top Abstract IntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
and RANTES activity. MC-21 and MC-68 efficiently blocked
the ligand binding to CCR2 and CCR5 with an IC50 of 0.09
and 0.6–1.0 µg/ml, respectively. In good correlation to these in
vitro data, MC-21 almost completely prevented the influx of monocytes
in thioglycollate-induced peritonitis. Therefore, both Abs appear as
useful reagents to further study the role of CCR2 and CCR5 in murine
disease models. |
Introduction |
|---|
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
(12, 13) and IL-12
(10). An association of chemokine receptors with Th1 and
Th2 cells has also been found in humans, where CCR5 and CXCR3 are
primarily expressed on Th1 cells (20), whereas CCR3, CCR4,
and CCR8 predominate on Th2 cells (21, 22, 23). Apart from knockout mice, chemokine receptor antagonists were used to study the role of chemokines in various models of inflammation. The chemokine analog methionine (Met)3-RANTES together with an antiserum against monocyte chemotactic protein (MCP)-1 was used in crescentic nephritis and resulted in a significant reduction of leukocyte infiltration, proteinuria, and tissue damage (24). Met-RANTES (3) showed a beneficial effect in collagen-induced arthritis (25) and the MCP-1 analog (MCP-1 9-76) prevented arthritis in the MRL-lpr mouse (26). Experimental nephritis in rats was improved by the virally encoded broad-spectrum chemokine antagonist macrophage-inflammatory protein (MIP)-II (4, 27) and the RANTES analog aminooxypentane (AOP)-RANTES (5, 28). Interpretation of those experiments is often difficult because chemokine analogs might bind to more than one chemokine receptor and the activity of most chemokine analogs has not been fully characterized on murine receptors. To better understand the effects of various chemokines and chemokine analogs on murine receptors, we analyzed ligand-induced internalization of CCR5 and CCR2 and determined the agonistic profile of various ligands.
The problem arising with the ill-defined receptor specificity of chemokine analogs could be overcome with receptor-specific inhibitory mAbs. Therefore, we investigated the inhibitory potential of our Abs and found a robust blockade of CCR2 and CCR5 with two of the clones.
|
Materials and Methods |
|---|
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
Chinese hamster ovary (CHO) (6) cells were stably
transfected with murine CCR2 (29) or CCR5 (30, 31) using the eucaryotic expression vector PEF-DHFR
(32). The coding region of the receptors was amplified
from genomic DNA and subcloned in the vector PEF-DHFR with
XbaI and SalI. Transfected CHO cells were
selected in nucleoside-free medium (-MEM; Life Technologies,
Rockville, MD) and expression of the receptors was further amplified by
addition of increasing concentrations of methotrexate. The cells were
cloned several times and expression of CCR2 and CCR5 was quantified
with a serum generated in rabbits against N-terminal peptides of the
receptors.
The murine chemokines MIP-1 and MCP-1 were obtained from R&D Systems
(Minneapolis, MN) and 125I-labeled chemokines
from Amersham Pharmacia (Uppsala, Sweden). Met-RANTES and AOP-RANTES
were produced as described (33, 34).
Generation of mAbs in rats
Wistar rats were immunized with at least six intraperitoneal injections of 107 transfected CHO cells in 3- to 4-wk intervals. Four days after the last injection, the spleens were removed and splenocytes fused to X63-Ag8 plasmocytoma cells. The resulting hybrids were plated on six 96-well plates at an approximate frequency of 10 clones/well. Positive clones were identified by FACS analysis on transfected and nontransfected CHO cells and cloned twice by limited dilution.
Preparation of cells and FACS analysis
Blood was obtained from anesthetized mice by puncture of the retro-orbital plexus or by cardiac puncture. Leukocytes were isolated from the kidneys using a slightly modified protocol as described by Cook et al. (35). Trypsin was omitted in the isolation procedure to avoid degradation of cell surface Ags, especially CD4 and CD8.
For FACS analysis, anti-coagulated full blood was incubated with 5 µg/ml of the mAbs MC-21 or MC-68 for 60 min on ice. Isotype controls (rat IgG2b; BD PharMingen, San Diego, CA) were always included in the assays. After three washing steps, the cells were incubated for 1 h on ice with a biotin-labeled anti-rat polyclonal Ab (Dako, Hamburg, Germany, and BD PharMingen) followed by PE-labeled streptavidin (Dako) and a combination of directly conjugated Abs. These were CD11b fluorescein-isothiocyanate (clone M1/70), CD8 Cy-Chrome and CD4 allophycocyanin, or Pan-NK FITC (clone DX-5), CD8 Cy-Chrome, and CD4 allophycocyanin (BD PharMingen). After lysis of erythrocytes with FACS lysing solution (Becton Dickinson, Franklin Lakes, NJ), the cells were analyzed on a flow cytometer (FACSCalibur; Becton Dickinson). Monocytes were identified by their light-scatter properties and expression of CD11b. NK cells were identified by gating the lymphocyte population and expression of DX-5 and CD11b as well as absence of the T cell Ags CD4 and CD8. The cutoff to define chemokine receptor-positive cells was set according to the staining with the isotype control Ab.
Down-modulation of chemokine receptors
Anti-coagulated full blood was incubated for 30 min at 37°C with various concentrations of chemokines as described previously (36). Two samples were incubated with medium as control. The cells were then placed on ice and stained for chemokine receptor expression as described above. One of the medium controls was stained with an isotype control Ab. Relative surface expression of chemokine receptors was determined by [(mean channel chemokine] - (mean channel isotype control)]/[(mean channel medium) - (mean channel isotype control)]. To demonstrate that reduced surface expression of chemokine receptors is due to internalization of the receptor, we also incubated the cells in parallel with chemokines on ice. Under these conditions, the binding of the mAbs MC-21 and MC-68 was not significantly reduced, excluding a chemokine-mediated inhibition of Ab binding (data not shown).
To investigate whether MC-21 or MC-68 induce receptor internalization by themselves, we incubated murine leukocytes with the Abs for 30 min on ice or at 37°C and then measured surface expression of CCR2 and CCR5 as described above.
Chemokine binding assays
CHO transfectants expressing CCR2 and CCR5 were harvested at
80% confluence and detached using PBS containing 1 mM EDTA.
Equilibrium competition binding assays were conducted in 96-well plates
by preincubating 1 x 105 cells in 50 mM
HEPES (pH 7.2), containing 1 mM CaCl2, 5 mM
MgCl2, and 0.5% BSA (binding buffer), and
appropriate dilutions of the Abs in binding buffer, for 1 h on
ice. The radiolabeled chemokines used were
125I-labeled MCP-1 for CCR2 and
125I-labeled MIP-1
,
125I-labeled MIP-1, and
125I-labeled RANTES for CCR5, which were added to
a final concentration of 0.1 nM. The cells were incubated for an
additional 4 h on ice, and the unbound iodinated chemokine removed
by washing three times with 200 µl of ice-cold binding
buffer containing 0.5 M NaCl under aspiration. Scintillant (50 µl)
was added to each well and the plates counted in a scintillation
counter for 1 min per well. Data were analyzed using Grafit 3.01
software using the following equation: B =
B0/1 +
[L]/IC50.
Thioglycollate-induced peritonitis and apoferritin-induced glomerulonephritis
For the induction of peritonitis in BALB/c mice, Brewer-Thioglycollate (1.5 ml, 4% solution in distilled water; Difco, Detroit, MI) was injected i.p. Before this injection, the treatment group (three mice) received 500 µg of MC-21 and the control group (three mice) received the same volume of PBS as i.p. injection. After 3 days, a peritoneal lavage was performed with ice-cold PBS containing 1 mM EDTA. The recovered cells were counted with a cell counter (Coulter Counter; Coulter Pharmaceutical, Palo Alto, CA) and monocytes/macrophages were identified by flow cytometry using light-scatter properties.
Immune complex-mediated glomerulonephritis was induced in BALB/c mice by daily i.p. injections of 4 mg of horse spleen apoferritin (Aldrich Chemical, Steinheim, Germany) in 80 µl of 0.1 M of sodium chloride as described (37). After 14 days, the kidneys were removed and leukocytes isolated and stained as described above. All animal experiments were approved by the governmental boards.
|
Results |
|---|
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
Rats were immunized with CHO cells stably transfected with murine CCR2 or CCR5. By several rounds of amplification and cloning, we obtained CHO cell clones with a high expression of chemokine receptors. A high receptor density is considered important for successful immunization. Chemokine receptor expression was quantified by FACS analysis using an antiserum generated in rabbits against N-terminal peptides of CCR2 or CCR5.
From 23 fusion reactions we identified 3 mAbs against CCR2 and 15 mAbs against CCR5. The Ab MC-21 directed against CCR2 and the Ab MC-68 directed against CCR5 (both IgG-2b) showed the best binding properties and were used for further analysis.
The specificity of the Abs was determined on CHO cells overexpressing
closely related human and murine chemokine receptors (Fig. 1
). The clone MC-21 binds to murine CCR2
but does not cross-react with murine CCR5 or human CCR2 and CCR5.
Similarly, the clone MC-68 only binds to murine CCR5 and not to murine
CCR2 or the human homologues. In addition, both Abs showed no
detectable binding to human PBMC. Further evidence for the specificity
of the mAbs is obtained with down-modulation experiments described
below.
|
A central aim of our study was to compare the chemokine receptor
expression in mice and humans. The mAbs MC-21 and MC-68 showed
excellent binding to CCR2 and CCR5, respectively, on primary mouse
leukocytes (Fig. 2). To further verify
that both Abs indeed recognize the appropriate chemokine receptors, we
induced internalization of the receptors with murine MCP-1 and murine
MIP-1 in parallel assays. The Abs MC-21 and MC-68 did not induce
receptor internalization by themselves (data not shown).
|
A, left). Moreover, the
expression level for CCR2 was higher on Th cells than on CTLs.
Monocytes stained homogeneously positive for CCR2. Preincubation with
murine MCP-1 caused a marked down-modulation of CCR2 (Fig. 2A, right).
In contrast, the expression pattern of CCR5 significantly differed
between the two species. Murine NK cells (DX-5+,
CD11b+, CD4-,
CD8-) homogeneously express high levels of CCR5
(Fig. 2B), whereas only a small subpopulation of human NK
cells weakly express CCR5 (1). The CCR5 expression on T
cells and monocytes was comparable in both species (38, 39). In mice, CCR5 is also expressed on a higher percentage of
CD8+ T cells (10–40%) than on
CD4+ T cells (3–10%) and freshly isolated
monocytes very weakly express CCR5 (Fig. 2B,
left). Down-modulation of CCR5 with MIP-1 almost
completely prevented binding of the Ab (Fig. 2B,
right).
In addition, we compared the CCR5 and CCR2 expression on leukocytes isolated from the peripheral blood, spleen, and lymph nodes of two different mouse strains, namely BALB/c and C57BL/6. The fraction of CCR5-positive T cells was somewhat higher in the spleen than in the two other compartments. Interestingly, the two strains differed in their chemokine receptor expression, because the percentage of CCR5- and CCR2-positive T cells was almost two times higher in the Th1-prone C57BL/6 mice than in the Th2-prone BALB/c mice (data not shown).
Blockade of CCR2 with the Ab MC-21 inhibition of thioglycollate-induced peritonitis
To analyze a potential blockade of CCR2 by the mAb MC-21, we
studied the inhibition of MCP-1-induced receptor internalization. As
shown in Figs. 2A and 3, murine MCP-1 efficiently
down-modulates CCR2 from the surface of T cells and monocytes. At a
concentration of 100 ng/ml, 
50% of CCR2 is internalized within 30
min at 37°C. Parallel incubation of cells on ice served as control to
exclude a sterical blockade of MC-21 binding by MCP-1 (Fig. 3A). A representative
histogram showing the internalization of CCR2 on monocytes with 1
µg/ml of MCP-1 is depicted in Fig. 3B.
|
A). When monocytes were
preincubated with 10 µg/ml of MC-21, only 14% of the surface CCR2
could be internalized by 250 ng/ml of MCP-1, whereas 80% of the
receptors were internalized in the absence of MC-21.
|
B).
To demonstrate that the Ab MC-21 is able to block CCR2 in vivo, we
studied the effect of MC-21 on thioglycollate-induced peritonitis.
Experiments with CCR2 knockout mice have demonstrated that CCR2 is
essential for the influx of monocytes/macrophages into the peritoneal
cavity in this model (13, 14, 15). Shortly before injection of
thioglycollate, we injected either 500 µg of MC-21 or PBS as a
control. After 3 days a peritoneal lavage was performed and the total
number of cells counted. As shown in Fig. 5A, treatment of mice with
MC-21 significantly reduced the number of peritoneal leukocytes. In an
additional experiment, we determined the relative number of
lymphocytes, granulocytes, and monocytes/macrophages in the peritoneal
lavage by flow cytometry (Fig. 5B). Treatment with MC-21
decreased the total number of monocytes/macrophages in the peritoneal
fluid by >90% (MC-21 group 7.0 x 106 vs
control 0.55 x 106; p <
0.001). In contrast, treatment with MC-21 had little influence on the
number of infiltrating granulocytes and lymphocytes indicating that
MC-21 efficiently blocks CCR2 in vivo and that the influx of
monocytes/macrophages is dependent on CCR2.
|
Down-modulation of CCR5 by various chemokines and the inhibitory effect of MC-68 were measured on murine peripheral blood leukocytes. Quantitative down-modulation of CCR5 was determined on NK cells because these cells homogeneously express high levels of CCR5. Comparable results were also obtained for T cells.
From all chemokines tested, murine MIP-1 most efficiently
internalized CCR5 (Fig. 6A).
It is approximately one order of magnitude more active than the two
human chemokines RANTES and MIP-1. More than sixty percent of
surface CCR5 was internalized with 12 ng/ml of murine MIP-1, whereas
>200 ng/ml of human RANTES were necessary for a comparable degree of
internalization. A representative histogram shows the internalization
of CCR5 on NK cells with 1 µg/ml MIP-1 (Fig. 6B). The
ability of MIP-1, MIP-1, and RANTES to induce receptor
internalization correlates well with their activity in Ca-flux
experiments (30). The two N-terminal modifications of
RANTES, Met-RANTES, and AOP-RANTES were also included in the assay
because they are commonly used as antagonists in rodent studies.
Met-RANTES and AOP-RANTES were approximately an order of magnitude less
efficient than unmodified RANTES or human MIP-1, indicating that the
modified versions of RANTES have only a weak agonistic activity on
murine CCR5. Met-RANTES and AOP-RANTES bind to murine CCR5 with about
the same affinity as unmodified RANTES (A.E.I.P., unpublished
observations).
|
(Fig. 7A). For that purpose, murine
blood cells were preincubated with MC-68 at a concentration of 10
µg/ml followed by incubation with various concentrations of the
chemokines. Internalization of CCR5 with both chemokines was
significantly blocked by MC-68. Internalization of CCR5 with 1 µg/ml
of RANTES was reduced from >80% to <20% by MC-68. Comparable
results were obtained for murine MIP-1 (100 ng/ml), where MC-68
reduced the internalization of CCR5 from 96% to 20%.
|
to
CCR5 was blocked with an IC50 of 0.6 µg/ml
(Fig. 7B). MC-68 also blocked the binding of MIP-1 and
RANTES with an IC50 of 1 µg/ml (data not
shown). These results indicate that MC-68 is a suitable reagent to
specifically block CCR5. Expression of CCR2/CCR5 on T cells in apoferritin-induced glomerulonephritis
A detailed knowledge of chemokine receptor expression in murine models of inflammation can provide important insights into the pathogenesis of certain diseases and help to fully understand the results obtained with knockout mice and receptor blockade by chemokine-analogs or small molecular antagonists. Moreover, we were interested whether in mice an accumulation of CCR5- and CCR2-positive cells is a hallmark for certain types of inflammation.
Therefore, we investigated the expression of CCR2 and CCR5 in a model
of immune complex-induced kidney inflammation, the apoferritin-induced
glomerulonephritis. Previously we have shown by RT-PCR and in situ
hybridization that both receptors are expressed in the kidneys
(37). Using FACS analysis, we now were able to quantify
the expression of both receptors on leukocytes isolated from the
peripheral blood and from the inflamed kidneys. As shown in Fig. 8, CCR5-positive and to a lesser extent
CCR2-positive T cells accumulate in the inflamed kidney. Although in
the peripheral blood only 3% of the CD4+ and
20% of the CD8+ T cells express CCR5, the
corresponding percentages in the kidney were 69% and 92%. A similar
distribution was found for CCR2, where only 4% of the
CD4+ and 3% of the CD8+ T
cells in the peripheral blood expressed CCR2 as opposed to 63% and
30% in the kidney with glomerulonephritis.
|
|
Discussion |
|---|
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
In humans the chemokine receptors CCR5 and CCR2 are highly expressed in chronic inflammation. In various types of arthritis, we found an accumulation of CCR5- and CCR2-positive T cells in the inflamed joints compared with their frequency in the peripheral blood (1). Both receptors also predominate on T cells in inflammatory kidney diseases including transplant rejection (6). In addition, multiple sclerosis (4, 5) and inflammatory bowel disease (7) are characterized by an accumulation of CCR5-positive cells. To demonstrate that a comparable enrichment of CCR2- and CCR5-positive T cells can be found in the inflamed kidneys of mice, we used the model of apoferritin-induced glomerulonephritis. FACS analysis of T cells isolated from the peripheral blood and the inflamed kidneys allowed a precise quantification of the percentage of CCR2- and CCR5-positive cells in both compartments. Although only 4% or 8% of the T cells in the peripheral blood expressed CCR2 or CCR5, respectively, the respective percentages in the inflamed kidney were 49% and 76%, corresponding to a 10-fold enrichment of CCR2- and CCR5-positive T cells. These data indicate that in mice a pronounced accumulation of CCR5- and CCR2-positive T cells also occurs after an inflammatory stimulus and that the roles of both chemokine receptors for T cells appear to be conserved in both species. Moreover, we found that the percentage of CCR5- and CCR2-positive T cells is almost two times higher in the Th1-prone mouse strain C57BL/6 than in the Th2-prone strain BALB/c. The strain-dependent expression correlates to a reduced Th1 response described in CCR5- and CCR2-deficient mice.
Using internalization assays with primary cells, we analyzed the
activation of CCR2 and CCR5 by various chemokines and chemokine
analogs. In most cases, internalization of chemokine receptors shows a
good correlation to other activation assays such as Ca-influx or
migration (36). The RANTES analog, Met-RANTES, has been
used extensively to block chemokine receptors in mice, whereas the
potent anti-HIV analog, AOP-RANTES, is less well documented for its
anti-inflammatory properties, although several studies are
currently ongoing. The results of these experiments are often difficult
to interpret because little is known about the effects of these
reagents on murine CCR5, and some of the reagents may influence
receptors other than CCR5. To get insight into the first issue, we
performed down-modulation assays measuring the agonistic activity of
various chemokines. On murine CCR5, the murine chemokine MIP-1 shows
a >10-fold higher activity than the two human chemokines RANTES and
MIP-1. The chemokine analogs Met-RANTES and AOP-RANTES were 100-fold
less active than murine MIP-1. Interestingly, the effect of
AOP-RANTES on murine CCR5 differs completely from its effect on
human CCR5, because AOP-RANTES efficiently internalizes the human
receptor (36) but is only weakly active on the murine
receptor. AOP-RANTES and Met-RANTES were shown to suppress disease
activity in models of experimental nephritis (28) and
collagen-induced arthritis (25). Consistent with these
findings, we show that both ligands are 100-fold less active on CCR5
than MIP-1 as measured by receptor internalization. Because
AOP-RANTES and Met-RANTES bind with about the same affinity to CCR5
(A.E.I.P., unpublished observations), the two RANTES analogs may be
considered CCR5 antagonists.
The mAbs MC-21 and MC-68 show a profound blockade of CCR2 and CCR5,
respectively. As described above, chemokine analogs often have the
disadvantage of acting on several receptors and knockout mice might
have partially adapted to the lifelong deficiency of the receptor. mAbs
would allow to specifically block one receptor at any given time point.
Therefore, we investigated whether the Abs MC-21 and MC-68 are able to
block ligand binding and activation of CCR2 and CCR5 measured by
chemokine-induced receptor internalization. The Ab MC-21 blocked the
binding of MCP-1 to murine CCR2 with an IC50 of
0.09 µg/ml. When murine monocytes were preincubated with MC-21, 20
times more MCP-1 was necessary to obtain the same degree of receptor
internalization as in the absence of MC-21 indicating that MC-21 blocks
nearly 95% of the MCP-1 activity. In good correlation to these in
vitro data, MC-21 almost completely prevented the influx of monocytes
in the model of thioglycollate-induced peritonitis, whereas the influx
of granulocytes and lymphocytes was not significantly altered. This
indicates that MC-21 efficiently blocks CCR2 in vivo and that the
influx of monocytes in contrast to other leukocytes is dependent on the
expression of CCR2.
We could also show that the Ab MC-68 efficiently blocks murine CCR5.
The binding of MIP-1, MIP-1, and RANTES was blocked with an
IC50 between 0.6 and 1.0 µg/ml. In addition
MC-68 neutralized >99% of the MIP-1 and RANTES activity as
measured by receptor internalization assays. Therefore, MC-68 appears
as useful reagent for inhibition of CCR5.
The mAbs against murine CCR2 and CCR5 are valuable tools to further study the role of these receptors in mice and to recognize potential limitations when transferring results from murine models to human diseases.
|
Acknowledgments |
|---|
|
Footnotes |
|---|
2 Address correspondence and reprint requests to Dr. Matthias Mack, Medical Policlinic, University of Munich, Pettenkoferstrasse 8a, 80336, Munich, Germany.
3 Abbreviations used in this paper: Met, methionine; MCP, monocyte chemotactic protein; MIP, macrophage-inflammatory protein; AOP, aminooxypentane; CHO, Chinese hamster ovary.
Received for publication August 22, 2000. Accepted for publication January 22, 2001.
|
References |
|---|
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
and IP-10 are expressed in demyelinating brain lesions. Proc. Natl. Acad. Sci. USA 96:6873.+ dendritic cells. Nat. Immun. 1:83.[Medline]
receptors: evidence for two closely linked C-C chemokine receptors on chromosome 9. J. Biol. Chem. 271:7551. receptor. J. Biol. Chem. 271:14445.This article has been cited by other articles:
|
|
 |
|
  A. Mildner, M. Mack, H. Schmidt, W. Bruck, M. Djukic, M. D. Zabel, A. Hille, J. Priller, and M. Prinz CCR2+Ly-6Chi monocytes are crucial for the effector phase of autoimmunity in the central nervous system Brain, June 16, 2009; (2009) awp144v1. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. M. Manicone, T. P. Birkland, M. Lin, T. Betsuyaku, N. van Rooijen, J. Lohi, J. Keski-Oja, Y. Wang, S. J. Skerrett, and W. C. Parks Epilysin (MMP-28) Restrains Early Macrophage Recruitment in Pseudomonas aeruginosa Pneumonia J. Immunol., March 15, 2009; 182(6): 3866 - 3876. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Herold, M. Steinmueller, W. von Wulffen, L. Cakarova, R. Pinto, S. Pleschka, M. Mack, W. A. Kuziel, N. Corazza, T. Brunner, et al. Lung epithelial apoptosis in influenza virus pneumonia: the role of macrophage-expressed TNF-related apoptosis-inducing ligand J. Exp. Med., December 22, 2008; 205(13): 3065 - 3077. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.-E. Turner, H.-J. Paust, O. M. Steinmetz, A. Peters, C. Meyer-Schwesinger, F. Heymann, U. Helmchen, S. Fehr, R. Horuk, U. Wenzel, et al. CCR5 Deficiency Aggravates Crescentic Glomerulonephritis in Mice J. Immunol., November 1, 2008; 181(9): 6546 - 6556. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. M. Handel, Z. Johnson, D. H. Rodrigues, A. C. dos Santos, R. Cirillo, V. Muzio, S. Riva, M. Mack, M. Deruaz, F. Borlat, et al. An engineered monomer of CCL2 has anti-inflammatory properties emphasizing the importance of oligomerization for chemokine activity in vivo J. Leukoc. Biol., October 1, 2008; 84(4): 1101 - 1108. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Varga, J. Ehrchen, A. Tsianakas, K. Tenbrock, A. Rattenholl, S. Seeliger, M. Mack, J. Roth, and C. Sunderkoetter Glucocorticoids induce an activated, anti-inflammatory monocyte subset in mice that resembles myeloid-derived suppressor cells J. Leukoc. Biol., September 1, 2008; 84(3): 644 - 650. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Mildner, M. Djukic, D. Garbe, A. Wellmer, W. A. Kuziel, M. Mack, R. Nau, and M. Prinz Ly-6G+CCR2- Myeloid Cells Rather Than Ly-6ChighCCR2+ Monocytes Are Required for the Control of Bacterial Infection in the Central Nervous System J. Immunol., August 15, 2008; 181(4): 2713 - 2722. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Yahiaoui, D. Gvozdic, G. Danialou, M. Mack, and B. J. Petrof CC family chemokines directly regulate myoblast responses to skeletal muscle injury J. Physiol., August 15, 2008; 586(16): 3991 - 4004. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. B. Sanz, P. Justo, M. D. Sanchez-Nino, L. M. Blanco-Colio, J. A. Winkles, M. Kreztler, A. Jakubowski, J. Blanco, J. Egido, M. Ruiz-Ortega, et al. The Cytokine TWEAK Modulates Renal Tubulointerstitial Inflammation J. Am. Soc. Nephrol., April 1, 2008; 19(4): 695 - 703. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. E. Orwig, B.-Y. Ryu, S. R. Master, B. T. Phillips, M. Mack, M. R. Avarbock, L. Chodosh, and R. L. Brinster Genes Involved in Post-Transcriptional Regulation Are Overrepresented in Stem/Progenitor Spermatogonia of Cryptorchid Mouse Testes Stem Cells, April 1, 2008; 26(4): 927 - 938. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Gupta, B. Fuchs, S. Schulz-Maronde, A. Heitland, S. E. Escher, M. Mack, H.-C. Tillmann, A. Braun, W.-G. Forssmann, J. Elsner, et al. Intravascular inactivation of CCR5 by n-Nonanoyl-CC chemokine ligand 14 and inhibition of allergic airway inflammation J. Leukoc. Biol., March 1, 2008; 83(3): 765 - 773. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Jakubzick, F. Tacke, F. Ginhoux, A. J. Wagers, N. van Rooijen, M. Mack, M. Merad, and G. J. Randolph Blood Monocyte Subsets Differentially Give Rise to CD103+ and CD103- Pulmonary Dendritic Cell Populations J. Immunol., March 1, 2008; 180(5): 3019 - 3027. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. W. Choi, G. C. Hildebrandt, K. M. Olkiewicz, D. A. Hanauer, M. N. Chaudhary, I. A. Silva, C. E. Rogers, D. T. Deurloo, J. M. Fisher, C. Liu, et al. CCR1/CCL5 (RANTES) receptor-ligand interactions modulate allogeneic T-cell responses and graft-versus-host disease following stem-cell transplantation Blood, November 1, 2007; 110(9): 3447 - 3455. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Winter, K. Taut, F. Langer, M. Mack, D. E. Briles, J. C. Paton, R. Maus, M. Srivastava, T. Welte, and U. A. Maus FMS-Like Tyrosine Kinase 3 Ligand Aggravates the Lung Inflammatory Response to Streptococcus pneumoniae Infection in Mice: Role of Dendritic Cells J. Immunol., September 1, 2007; 179(5): 3099 - 3108. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
O. Kulkarni, R. D. Pawar, W. Purschke, D. Eulberg, N. Selve, K. Buchner, V. Ninichuk, S. Segerer, V. Vielhauer, S. Klussmann, et al. Spiegelmer Inhibition of CCL2/MCP-1 Ameliorates Lupus Nephritis in MRL-(Fas)lpr Mice J. Am. Soc. Nephrol., August 1, 2007; 18(8): 2350 - 2358. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 U. A. Maus, M. Backi, C. Winter, M. Srivastava, M. K. Schwarz, T. Ruckle, J. C. Paton, D. Briles, M. Mack, T. Welte, et al. Importance of Phosphoinositide 3-Kinase {gamma} in the Host Defense against Pneumococcal Infection Am. J. Respir. Crit. Care Med., May 1, 2007; 175(9): 958 - 966. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Thapa, W. A. Kuziel, and D. J. J. Carr Susceptibility of CCR5-Deficient Mice to Genital Herpes Simplex Virus Type 2 Is Linked to NK Cell Mobilization J. Virol., April 15, 2007; 81(8): 3704 - 3713. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Wendland, N. Czeloth, N. Mach, B. Malissen, E. Kremmer, O. Pabst, and R. Forster CCR9 is a homing receptor for plasmacytoid dendritic cells to the small intestine PNAS, April 10, 2007; 104(15): 6347 - 6352. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. D. Wareing, A. Lyon, C. Inglis, F. Giannoni, I. Charo, and S. R. Sarawar Chemokine regulation of the inflammatory response to a low-dose influenza infection in CCR2-/- mice J. Leukoc. Biol., March 1, 2007; 81(3): 793 - 801. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Sawaki, H. Tsutsui, N. Hayashi, K. Yasuda, S. Akira, T. Tanizawa, and K. Nakanishi Type 1 cytokine/chemokine production by mouse NK cells following activation of their TLR/MyD88-mediated pathways Int. Immunol., March 1, 2007; 19(3): 311 - 320. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. M. Conrad, D. Strauss-Ayali, A. E. Field, M. Mack, and D. M. Mosser Leishmania-Derived Murine Monocyte Chemoattractant Protein 1 Enhances the Recruitment of a Restrictive Population of CC Chemokine Receptor 2-Positive Macrophages Infect. Immun., February 1, 2007; 75(2): 653 - 665. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Yasuda, T. Kuwabara, H. Nakano, K. Aritomi, T. Onodera, M. Lipp, Y. Takahama, and T. Kakiuchi Chemokines CCL19 and CCL21 promote activation-induced cell death of antigen-responding T cells Blood, January 15, 2007; 109(2): 449 - 456. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. Moreno, C. Nicaise, T. Gustot, E. Quertinmont, N. Nagy, M. Parmentier, H. Louis, and J. Deviere Chemokine receptor CCR5 deficiency exacerbates cerulein-induced acute pancreatitis in mice Am J Physiol Gastrointest Liver Physiol, December 1, 2006; 291(6): G1089 - G1099. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Engel, U. Dobrindt, A. Tittel, P. Peters, J. Maurer, I. Gutgemann, B. Kaissling, W. Kuziel, S. Jung, and C. Kurts Tumor Necrosis Factor Alpha- and Inducible Nitric Oxide Synthase-Producing Dendritic Cells Are Rapidly Recruited to the Bladder in Urinary Tract Infection but Are Dispensable for Bacterial Clearance Infect. Immun., November 1, 2006; 74(11): 6100 - 6107. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. K. Henke, C. G. Pearce, D. M. Moaveni, A. J. Moore, E. M. Lynch, C. Longo, M. Varma, N. A. Dewyer, K. B. Deatrick, G. R. Upchurch Jr, et al. Targeted Deletion of CCR2 Impairs Deep Vein Thombosis Resolution in a Mouse Model. J. Immunol., September 1, 2006; 177(5): 3388 - 3397. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Herold, W. von Wulffen, M. Steinmueller, S. Pleschka, W. A. Kuziel, M. Mack, M. Srivastava, W. Seeger, U. A. Maus, and J. Lohmeyer Alveolar Epithelial Cells Direct Monocyte Transepithelial Migration upon Influenza Virus Infection: Impact of Chemokines and Adhesion Molecules J. Immunol., August 1, 2006; 177(3): 1817 - 1824. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Zhang, D. Yang, H. Dong, Q. Chen, D. I. Dimitrova, T. J. Rogers, M. Sitkovsky, and J. J. Oppenheim Adenosine A2a receptors induce heterologous desensitization of chemokine receptors Blood, July 1, 2006; 108(1): 38 - 44. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Stenstad, A. Ericsson, B. Johansson-Lindbom, M. Svensson, J. Marsal, M. Mack, D. Picarella, D. Soler, G. Marquez, M. Briskin, et al. Gut-associated lymphoid tissue-primed CD4+ T cells display CCR9-dependent and -independent homing to the small intestine Blood, May 1, 2006; 107(9): 3447 - 3454. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. Ma, W. Liu, R. J. Homer, P. J. Lee, A. J. Coyle, J. M. Lora, C. G. Lee, and J. A. Elias Role of CCR5 in the Pathogenesis of IL-13-Induced Inflammation and Remodeling. J. Immunol., April 15, 2006; 176(8): 4968 - 4978. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. J. J. Carr, J. Ash, T. E. Lane, and W. A. Kuziel Abnormal immune response of CCR5-deficient mice to ocular infection with herpes simplex virus type 1. J. Gen. Virol., March 1, 2006; 87(Pt 3): 489 - 499. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. J. Crane, H. Xu, C. Wallace, A. Manivannan, M. Mack, J. Liversidge, G. Marquez, P. F. Sharp, and J. V. Forrester Involvement of CCR5 in the passage of Th1-type cells across the blood-retina barrier in experimental autoimmune uveitis J. Leukoc. Biol., March 1, 2006; 79(3): 435 - 443. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. L. Hardison, R. A. Wrightsman, P. M. Carpenter, W. A. Kuziel, T. E. Lane, and J. E. Manning The CC Chemokine Receptor 5 Is Important in Control of Parasite Replication and Acute Cardiac Inflammation following Infection with Trypanosoma cruzi Infect. Immun., January 1, 2006; 74(1): 135 - 143. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Nakayama, N. Mutsuga, L. Yao, and G. Tosato Prostaglandin E2 promotes degranulation-independent release of MCP-1 from mast cells J. Leukoc. Biol., January 1, 2006; 79(1): 95 - 104. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. A. Reichel, A. Khandoga, H.-J. Anders, D. Schlondorff, B. Luckow, and F. Krombach Chemokine receptors Ccr1, Ccr2, and Ccr5 mediate neutrophil migration to postischemic tissue J. Leukoc. Biol., January 1, 2006; 79(1): 114 - 122. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. P. de Lema, H. Maier, T. J. Franz, M. Escribese, S. Chilla, S. Segerer, N. Camarasa, H. Schmid, B. Banas, S. Kalaydjiev, et al. Chemokine Receptor Ccr2 Deficiency Reduces Renal Disease and Prolongs Survival in MRL/lpr Lupus-Prone Mice J. Am. Soc. Nephrol., December 1, 2005; 16(12): 3592 - 3601. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Xu, A. Manivannan, R. Dawson, I. J. Crane, M. Mack, P. Sharp, and J. Liversidge Differentiation to the CCR2+ Inflammatory Phenotype In Vivo Is a Constitutive, Time-Limited Property of Blood Monocytes and Is Independent of Local Inflammatory Mediators J. Immunol., November 15, 2005; 175(10): 6915 - 6923. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. S. Duffield, P. G. Tipping, T. Kipari, J.-F. Cailhier, S. Clay, R. Lang, J. V. Bonventre, and J. Hughes Conditional Ablation of Macrophages Halts Progression of Crescentic Glomerulonephritis Am. J. Pathol., November 1, 2005; 167(5): 1207 - 1219. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. H. Terwey, T. D. Kim, A. A. Kochman, V. M. Hubbard, S. Lu, J. L. Zakrzewski, T. Ramirez-Montagut, J. M. Eng, S. J. Muriglan, G. Heller, et al. CCR2 is required for CD8-induced graft-versus-host disease Blood, November 1, 2005; 106(9): 3322 - 3330. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. A. Wysocki, A. Panoskaltsis-Mortari, B. R. Blazar, and J. S. Serody Leukocyte migration and graft-versus-host disease Blood, June 1, 2005; 105(11): 4191 - 4199. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. L. Hokeness, W. A. Kuziel, C. A. Biron, and T. P. Salazar-Mather Monocyte Chemoattractant Protein-1 and CCR2 Interactions Are Required for IFN-{alpha}/{beta}-Induced Inflammatory Responses and Antiviral Defense in Liver J. Immunol., February 1, 2005; 174(3): 1549 - 1556. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 U. A. Maus, S. Wellmann, C. Hampl, W. A. Kuziel, M. Srivastava, M. Mack, M. B. Everhart, T. S. Blackwell, J. W. Christman, D. Schlondorff, et al. CCR2-positive monocytes recruited to inflamed lungs downregulate local CCL2 chemokine levels Am J Physiol Lung Cell Mol Physiol, February 1, 2005; 288(2): L350 - L358. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Mack, M. A. Schneider, C. Moll, J. Cihak, H. Bruhl, J. W. Ellwart, M. P. Hogarth, M. Stangassinger, and D. Schlondorff Identification of Antigen-Capturing Cells as Basophils J. Immunol., January 15, 2005; 174(2): 735 - 741. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B.-C. Chiu, C. M. Freeman, V. R. Stolberg, J. S. Hu, K. Zeibecoglou, B. Lu, C. Gerard, I. F. Charo, S. A. Lira, and S. W. Chensue Impaired Lung Dendritic Cell Activation in CCR2 Knockout Mice Am. J. Pathol., October 1, 2004; 165(4): 1199 - 1209. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. M. Scott Algood and J. L. Flynn CCR5-Deficient Mice Control Mycobacterium tuberculosis Infection despite Increased Pulmonary Lymphocytic Infiltration J. Immunol., September 1, 2004; 173(5): 3287 - 3296. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Rodriguez-Sosa, R. Saavedra, E. P. Tenorio, L. E. Rosas, A. R. Satoskar, and L. I. Terrazas A STAT4-Dependent Th1 Response Is Required for Resistance to the Helminth Parasite Taenia crassiceps Infect. Immun., August 1, 2004; 72(8): 4552 - 4560. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. Peters, J. G. Cyster, M. Mack, D. Schlondorff, A. J. Wolf, J. D. Ernst, and I. F. Charo CCR2-Dependent Trafficking of F4/80dim Macrophages and CD11cdim/intermediate Dendritic Cells Is Crucial for T Cell Recruitment to Lungs Infected with Mycobacterium tuberculosis J. Immunol., June 15, 2004; 172(12): 7647 - 7653. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. C. Hildebrandt, U. A. Duffner, K. M. Olkiewicz, L. A. Corrion, N. E. Willmarth, D. L. Williams, S. G. Clouthier, C. M. Hogaboam, P. R. Reddy, B. B. Moore, et al. A critical role for CCR2/MCP-1 interactions in the development of idiopathic pneumonia syndrome after allogeneic bone marrow transplantation Blood, March 15, 2004; 103(6): 2417 - 2426. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Oostendorp, M. N. Hylkema, M. Luinge, M. Geerlings, H. Meurs, W. Timens, J. Zaagsma, D. S. Postma, H. W. Boddeke, and K. Biber Localization and Enhanced mRNA Expression of the Orphan Chemokine Receptor L-CCR in the Lung in a Murine Model of Ovalbumin-induced Airway Inflammation J. Histochem. Cytochem., March 1, 2004; 52(3): 401 - 410. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. Eis, B. Luckow, V. Vielhauer, J. T. Siveke, Y. Linde, S. Segerer, G. P. de Lema, C. D. Cohen, M. Kretzler, M. Mack, et al. Chemokine Receptor CCR1 But Not CCR5 Mediates Leukocyte Recruitment and Subsequent Renal Fibrosis after Unilateral Ureteral Obstruction J. Am. Soc. Nephrol., February 1, 2004; 15(2): 337 - 347. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
B. L. Colvin, A. E. Morelli, A. J. Logar, A. H. Lau, and A. W. Thomson Comparative evaluation of CC chemokine-induced migration of murine CD8{alpha}+ and CD8{alpha}- dendritic cells and their in vivo trafficking J. Leukoc. Biol., February 1, 2004; 75(2): 275 - 285. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Bruhl, J. Cihak, M. A. Schneider, J. Plachy, T. Rupp, I. Wenzel, M. Shakarami, S. Milz, J. W. Ellwart, M. Stangassinger, et al. Dual Role of CCR2 during Initiation and Progression of Collagen-Induced Arthritis: Evidence for Regulatory Activity of CCR2+ T Cells J. Immunol., January 15, 2004; 172(2): 890 - 898. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Penido, A. Vieira-de-Abreu, M. T. Bozza, H. C. Castro-Faria-Neto, and P. T. Bozza Role of Monocyte Chemotactic Protein-1/CC Chemokine Ligand 2 on {gamma}{delta} T Lymphocyte Trafficking during Inflammation Induced by Lipopolysaccharide or Mycobacterium bovis Bacille Calmette-Guerin J. Immunol., December 15, 2003; 171(12): 6788 - 6794. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. Lee, L. Wang, A. D. Wells, Q. Ye, R. Han, M. E. Dorf, W. A. Kuziel, B. J. Rollins, L. Chen, and W. W. Hancock Blocking the Monocyte Chemoattractant Protein-1/CCR2 Chemokine Pathway Induces Permanent Survival of Islet Allografts through a Programmed Death-1 Ligand-1-Dependent Mechanism J. Immunol., December 15, 2003; 171(12): 6929 - 6935. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. C. Robinson, K. A. Scott, J. L. Wilson, R. G. Thompson, A. E. I. Proudfoot, and F. R. Balkwill A Chemokine Receptor Antagonist Inhibits Experimental Breast Tumor Growth Cancer Res., December 1, 2003; 63(23): 8360 - 8365. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
Y. Chvatchko, A. E. I. Proudfoot, R. Buser, P. Juillard, S. Alouani, M. Kosco-Vilbois, A. J. Coyle, R. J. Nibbs, G. Graham, R. E. Offord, et al. Inhibition of Airway Inflammation by Amino-Terminally Modified RANTES/CC Chemokine Ligand 5 Analogues Is Not Mediated through CCR3 J. Immunol., November 15, 2003; 171(10): 5498 - 5506. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Crittenden, M. Gough, K. Harrington, K. Olivier, J. Thompson, and R. G. Vile Expression of Inflammatory Chemokines Combined with Local Tumor Destruction Enhances Tumor Regression and Long-term Immunity Cancer Res., September 1, 2003; 63(17): 5505 - 5512. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K.-H. Sonoda, Y. Sasa, H. Qiao, C. Tsutsumi, T. Hisatomi, S. Komiyama, T. Kubota, T. Sakamoto, Y.-I. Kawano, and T. Ishibashi Immunoregulatory Role of Ocular Macrophages: The Macrophages Produce RANTES to Suppress Experimental Autoimmune Uveitis J. Immunol., September 1, 2003; 171(5): 2652 - 2659. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Tsutsumi, K.-H. Sonoda, K. Egashira, H. Qiao, T. Hisatomi, S. Nakao, M. Ishibashi, I. F. Charo, T. Sakamoto, T. Murata, et al. The critical role of ocular-infiltrating macrophages in the development of choroidal neovascularization J. Leukoc. Biol., July 1, 2003; 74(1): 25 - 32. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
U. A. Maus, K. Waelsch, W. A. Kuziel, T. Delbeck, M. Mack, T. S. Blackwell, J. W. Christman, D. Schlondorff, W. Seeger, and J. Lohmeyer Monocytes Are Potent Facilitators of Alveolar Neutrophil Emigration During Lung Inflammation: Role of the CCL2-CCR2 Axis J. Immunol., March 15, 2003; 170(6): 3273 - 3278. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Onuffer, M. A. McCarrick, L. Dunning, M. Liang, M. Rosser, G.-P. Wei, H. Ng, and R. Horuk Structure Function Differences in Nonpeptide CCR1 Antagonists for Human and Mouse CCR1 J. Immunol., February 15, 2003; 170(4): 1910 - 1916. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H.-J. Anders, B. Banas, Y. Linde, L. Weller, C. D. Cohen, M. Kretzler, S. Martin, V. Vielhauer, D. Schlondorff, and H.-J. Grone Bacterial CpG-DNA Aggravates Immune Complex Glomerulonephritis: Role of TLR9-Mediated Expression of Chemokines and Chemokine Receptors J. Am. Soc. Nephrol., February 1, 2003; 14(2): 317 - 326. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Wolf, T. Jocks, G. Zahner, U. Panzer, and R. A. K. Stahl Existence of a regulatory loop between MCP-1 and TGF-beta in glomerular immune injury Am J Physiol Renal Physiol, November 1, 2002; 283(5): F1075 - F1084. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Zhang, M. P. Soares, Y. Guan, S. Matheravidathu, R. Wnek, K. E. Johnson, A. Meisher, S. A. Iliff, J. S. Mudgett, M. S. Springer, et al. Functional Expression and Characterization of Macaque C-C Chemokine Receptor 3 (CCR3) and Generation of Potent Antagonistic Anti-macaque CCR3 Monoclonal Antibodies J. Biol. Chem., September 6, 2002; 277(37): 33799 - 33810. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
U. Maus, K. von Grote, W. A. Kuziel, M. Mack, E. J. Miller, J. Cihak, M. Stangassinger, R. Maus, D. Schlondorff, W. Seeger, et al. The Role of CC Chemokine Receptor 2 in Alveolar Monocyte and Neutrophil Immigration in Intact Mice Am. J. Respir. Crit. Care Med., August 1, 2002; 166(3): 268 - 273. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Rodriguez-Sosa, A. R. Satoskar, R. Calderon, L. Gomez-Garcia, R. Saavedra, R. Bojalil, and L. I. Terrazas Chronic Helminth Infection Induces Alternatively Activated Macrophages Expressing High Levels of CCR5 with Low Interleukin-12 Production and Th2-Biasing Ability Infect. Immun., July 1, 2002; 70(7): 3656 - 3664. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. Tomiyama, T. Matsuda, and M. Takiguchi Differentiation of Human CD8+ T Cells from a Memory to Memory/Effector Phenotype J. Immunol., June 1, 2002; 168(11): 5538 - 5550. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 W. I. de Boer Cytokines and Therapy in COPD* : A Promising Combination? Chest, May 1, 2002; 121(5_suppl): 209S - 218S. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. VIELHAUER, H.-J. ANDERS, M. MACK, J. CIHAK, F. STRUTZ, M. STANGASSINGER, B. LUCKOW, H.-J. GRÖNE, and D. SCHLÖNDORFF Obstructive Nephropathy in the Mouse: Progressive Fibrosis Correlates with Tubulointerstitial Chemokine Expression and Accumulation of CC Chemokine Receptor 2- and 5-Positive Leukocytes J. Am. Soc. Nephrol., June 1, 2001; 12(6): 1173 - 1187. [Abstract] [Full Text]
|
|
|
|
|
|
U. A. Maus, M. A. Koay, T. Delbeck, M. Mack, M. Ermert, L. Ermert, T. S. Blackwell, J. W. Christman, D. Schlondorff, W. Seeger, et al. Role of resident alveolar macrophages in leukocyte traffic into the alveolar air space of intact mice Am J Physiol Lung Cell Mol Physiol, June 1, 2002; 282(6): L1245 - L1252. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
