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Interleukin‐4 promotes human CD8 + T cell expression of CCR7
Author(s) -
Seneviratne Suranjith L.,
Black Antony P.,
Jones Louise,
Di Gleria Kati,
Bailey Abigail S.,
Ogg Graham S.
Publication year - 2007
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2006.02478.x
Subject(s) - cd8 , cd28 , t cell , c c chemokine receptor type 7 , cytotoxic t cell , biology , immunology , antigen , cytokine , interleukin 21 , homing (biology) , microbiology and biotechnology , immune system , in vitro , chemokine , genetics , chemokine receptor , ecology
Summary Despite strong evidence supporting a pathway of human T cell differentiation characterized by changes in the expression of CCR7, CD28, CD27 and CD62L, few studies have addressed the mechanisms of pathway regulation. Cutaneous lymphocyte‐associated antigen (CLA)‐positive skin‐homing CD8 + T cells expressed significantly elevated levels of activation markers compared with CLA − CD8 + T cells in individuals ( n = 27) with cutaneous atopic disease. Despite such an activated phenotype, CLA + T cells expressed significantly higher levels of CCR7 than a CLA − T cell subset. Interleukin (IL)‐4 was found to dramatically promote CCR7 expression by antigen‐specific CD8 + cells. Furthermore, skin‐homing CD8 + T cells from individuals with severe disease produced significantly less IL‐10 than those derived from mildly affected atopic subjects. Thus in a T‐helper 2 dominated disease, tissue‐specific CD8 + T cells show altered CCR7 expression and cytokine production, which may contribute to continued lymph node homing, antigen presentation and disease. IL‐4 promotes expression of CCR7, a marker linked to existing models of CD8 + T cell differentiation.