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CCR7 Signaling Promotes T Cell Survival and Proliferation
Author(s) -
Li ChengRui Michael,
Lo David D
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.385
Subject(s) - microbiology and biotechnology , c c chemokine receptor type 7 , t cell , cell growth , biology , t cell receptor , cd8 , chemokine , immune system , immunology , chemokine receptor , biochemistry
T cells undergo homeostatic proliferation under states of lymphopenia in the body. Detailed molecular mechanisms regulating this phenomenon have not been completely elucidated. Our previous studies suggested that the homeostatic chemokine receptor, CCR7, may play a role in T cell homeostatic proliferation and autoimmunity induction. In this study, we tested if CCR7 signal itself stimulates T cell proliferation and/or if it promotes T cell survival in in vitro culture experiments with CCR7 ligands. The results show that, when purified T cells were cultured in the absence of TCR stimulation, more cells survived in the present of CCR7 ligands treatment, in a dose response manner, indicating that CCR7 signal can promote T cell survival. Interestingly, CD4 + T cells seemed to be more responsive to CCR7 ligand treatment than CD8 + T cells. Although signaling through CCR7 alone does not induce proliferation of ligand‐treated T cells, this treatment can increase anti‐CD3 induced T cell proliferation. However, CCR7 ligand treatment did not increase anit‐CD3 stimulated cytokine expression and CD44 upregulation, suggesting that CCR7 does not provide a bona fide co‐stimulation for T cell. These data suggest that signaling through CCR7 may positively modulate T cell homeostatic proliferation by enhancing signals from MHC/peptide and by promoting T cell survival.