CCR5 is characteristic of Th1 lymphocytes

Loetscher, Pius; Uguccioni, Mariagrazia; Bordoli, Lorenza; Baggiolini, Marco; Moser, Bernhard; Chizzolini, Carlo; Dayer, Jean‐Michel

doi:10.1038/34814

Cited by 782 publications

(485 citation statements)

References 2 publications

Supporting

Mentioning

453

Contrasting

Unclassified

Order By: Relevance

“…CCR5 positive T cells were found in each tissue sample analyzed as previously described for RA T cells [29,30], even though the number of CCR5 positive cells varied greatly in individual samples. CCR5 is expressed on effector/memory T cells and its expression is downregulated after T-cell activation [30].…”

Section: Discussionmentioning

confidence: 59%

“…Thus, the RA memory Th1 cells have irreversibly become committed to their phenotype as previously reported to occur when Th1 and Th2 cells are repeatedly stimulated [27,28]. In contrast to the fixed cytokine phenotype, another way to phenotypically characterize Th1 and Th2 cells is by the use of the chemokine receptor expression [14,29]. In this report we demonstrate that the Th2-chemokine receptor CCR3 can be induced in polarized memory Th1 clones and polyclonal Th1-cell lines, even though their cytokine profile is not altered.…”

Section: Discussionmentioning

confidence: 86%

See 1 more Smart Citation

Switch in Chemokine Receptor Phenotype on Memory T Cells without a Change in the Cytokine Phenotype

et al. 2001

View full text Add to dashboard Cite

Induction of CCR5 expression on Th2 clones was associated with secretion of some IFN-g. Moreover, the Th2-associated chemokine receptor CCR3 could be expressed on both Th1-dominant cell lines, and clones of Th1 and Th0 type after culture conditions with IL-4. This expression of CCR3 was associated with a reduced IFN-g production, but no IL-4 production could be induced. The IL-4-treated Th1 clones had a reduced migratory capacity against chemokines produced by ST cells compared to nonmanipulated T-cell clones. In contrast, the same IL-12-treated Th1 clones showed an increased migratory potential. Induction of the Th2-associated marker CCR3 on memory Th1 cells demonstrates that a change in chemokine receptor phenotype related to the Th2 type can be induced on terminally differentiated Th1 cells, without a change in the cytokine profile.

show abstract

Section: Discussionmentioning

confidence: 59%

Section: Discussionmentioning

confidence: 86%

Switch in Chemokine Receptor Phenotype on Memory T Cells without a Change in the Cytokine Phenotype

et al. 2001

View full text Add to dashboard Cite

show abstract

“…Expression of CCR5 on CD4 1 T lymphocytes has been associated with a Th1 immune response [40]. Subsequently, it was reported that Ccr5 deficiency results in a shift from a Th1 towards a Th2 response in mice with dextran sodium sulfate-induced colitis [41].…”

Section: Discussionmentioning

confidence: 99%

Chemokine receptor Ccr5 deficiency induces alternative macrophage activation and improves long‐term renal allograft outcome

et al. 2009

View full text Add to dashboard Cite

The chemokine (C-C motif) receptor 5 (CCR5) has been implicated in experimental and clinical allograft rejection. To dissect the function of CCR5 in acute and chronic renal allograft rejection, bilaterally nephrectomized WT and Ccr5 À/À C57BL/6 mice were used as recipients of WT BALB/c renal allografts and analyzed 7 and 42 days after transplantation. Lesion scores (glomerular damage, vascular rejection, tubulointerstitial inflammation) and numbers of CD4 1 , CD8 1 , CD11c 1 and alpha smooth muscle actin (aSMA) 1 cells were reduced in allografts from Ccr5 À/À recipients during the chronic phase. Increasing creatinine levels indicated deterioration of allograft function over time. While mRNA expression of Th1-associated markers decreased between 7 and 42 days, Th2-associated markers increased. Markers for alternatively activated macrophages (arginase 1, chitinase 3-like 3, resistin-like a, mannose receptor, C type 1), were strongly upregulated (mRNA and/or protein level) only in allografts from Ccr5 À/À recipients at 42 days. Ccr5 deficiency shifted intragraft immune responses during the chronic phase towards the Th2 type and led to accumulation of alternatively activated macrophages. Additionally, splenocytes from unchallenged Ccr5 À/À mice showed significantly increased arginase 1 and mannose receptor 1 mRNA levels, suggesting constitutive alternative activation of splenic macrophages. We conclude that Ccr5 deficiency favors alternative macrophage activation. This finding may be relevant for other inflammatory diseases that involve macrophage activation and may also influence future therapeutic strategies targeting CCR5.

show abstract

“…Since CCR5 expression is associated with Th1 cell polarization [25], IFN-+ -related mechanisms may contribute to the disease provoked by CCR5 + cells. Chemokine receptors including CCR5, as well as Th1 cytokines, were shown to be induced at high levels during islet allograft rejection [26].…”

Section: Discussionmentioning

confidence: 99%

Leukocyte attraction through the CCR5 receptor controls progress from insulitis to diabetes in non‐obese diabetic mice

et al. 2004

View full text Add to dashboard Cite

Lymphocyte infiltration to pancreatic islets is associated to chemoattraction, as are other inflammatory autoimmune processes. We examined whether development of insulitis and diabetes depends on chemoattraction of lymphocytes via the CCR5 chemokine receptor. In non-obese diabetic (NOD) mice, a substantial fraction of peripheral T cells and virtually all B cells expressed high CCR5 levels. CCR5 expression characterized the effector T cell phenotype, suggesting their potential involvement in disease development. In view of these findings and the CCL5 (RANTES, the CCR5 ligand) expression by pancreatic islets, we treated NOD mice with a neutralizing anti-CCR5 antibody. This did not influence peri-insulitis advancement, but inhibited g -cell destruction and diabetes. These data demonstrate a role of CCR5-dependent chemoattraction in insulitis progression to islet destruction, suggesting the potential value of therapeutic intervention by CCR5 targeting.

show abstract

CCR5 is characteristic of Th1 lymphocytes

Cited by 782 publications

References 2 publications

Switch in Chemokine Receptor Phenotype on Memory T Cells without a Change in the Cytokine Phenotype

Switch in Chemokine Receptor Phenotype on Memory T Cells without a Change in the Cytokine Phenotype

Chemokine receptor Ccr5 deficiency induces alternative macrophage activation and improves long‐term renal allograft outcome

Leukocyte attraction through the CCR5 receptor controls progress from insulitis to diabetes in non‐obese diabetic mice

Contact Info

Product

Resources

About