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Differential effects of CD4 and CD8 engagement on the development of cytokine profiles of murine CD4 + and CD8 + T lymphocytes
Author(s) -
Campbell S. B.,
Komata T.,
Kelso A.
Publication year - 2000
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2000.00971.x
Subject(s) - cytotoxic t cell , cd8 , cd28 , antibody , biology , antigen , microbiology and biotechnology , priming (agriculture) , cytokine , t lymphocyte , immunology , in vitro , biochemistry , botany , germination
Summary A simple culture system devoid of antigen‐presenting cells was used to examine the ability of immobilized antibodies to lymphocyte function‐associated antigen‐1 (LFA‐1) (CD11a), CD28 and CD4 or CD8 to modulate the responses of normal murine CD4 + and CD8 + lymph node T cells to immobilized anti‐CD3 antibody and interleukin‐2 (IL‐2). All the antibodies enhanced proliferative responses to limiting anti‐CD3 antibody. Both CD4 + and CD8 + cells produced substantial titres of IL‐3 and interferon‐γ (IFN‐γ) in primary and secondary cultures regardless of the coactivating antibodies used for priming. By contrast, the combination of anti‐CD4 with anti‐CD3 antibody stimulated significantly higher titres of IL‐4 than any other antibody combination in cultures of CD4 + cells. This CD4‐dependent IL‐4 response was induced in CD4 + T cells of naive (CD44 low ) phenotype and was similar in magnitude to the response induced by exogenous IL‐4 but, unlike the latter, was not associated with elevated IL‐3 synthesis. A comparable effect of anti‐CD8 antibodies on CD8 + cells was not observed: although IL‐4 production by CD8 + cells was induced by exogenous IL‐4, it was not detected following coactivation with anti‐CD8 or any other antibodies. We conclude that anti‐CD4 antibody is a potent inducer of IL‐4‐secreting CD4 + T cells whose effects can be distinguished from those of anti‐CD8 antibody on CD8 + T cells and from those of IL‐4 on either subset.