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CD8 + T cells produce IL‐2, which is required for CD4 + CD25 + T cell regulation of effector CD8 + T cell development for contact hypersensitivity responses
Author(s) -
Kish Danielle D.,
Gorbachev Anton V.,
Fairchild Robert L.
Publication year - 2005
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1189/jlb.0205069
Subject(s) - effector , biology , il 2 receptor , cd8 , microbiology and biotechnology , cytotoxic t cell , t cell , immunology , immune system , biochemistry , in vitro
Interleukin (IL)‐2 functions to promote, as well as down‐regulate, expansion of antigen‐reactive CD4 + and CD8 + T cells, but the role of IL‐2 in hapten‐specific CD8 + T cell priming for contact hypersensitivity (CHS) responses remains untested. Using enzyme‐linked immunospot to enumerate numbers of hapten‐specific CD4 + and CD8 + T cells producing IL‐2 in hapten‐sensitized mice, the number of IL‐2‐producing CD8 + T cells was tenfold that of CD4 + T cells. Hapten‐primed D4 + T cells produced low amounts of IL‐2 during culture with hapten‐presenting Langerhans cells, whereas production by hapten‐primed CD8 + T cells was fivefold greater. CD8 + T cells did not express CD25 during hapten priming, but treatment with anti‐IL‐2 or anti‐CD25 monoclonal antibodies during hapten sensitization increased hapten‐specific effector CD8 + T cells as well as the magnitude and duration of the CHS response. These results indicate that CD8 + T cells are the primary source of IL‐2 and that this IL‐2 is required for the function of a population of CD4 + CD25 + T cells to restrict the development of the hapten‐reactive effector CD8 + T cells that mediate CHS responses.
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