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Role of interleukin‐2 in superantigen‐induced T‐cell anergy
Author(s) -
William D. Cornwell,
Thomas J. Rogers
Publication year - 1999
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.1365-2567.1999.00627.x
Subject(s) - superantigen , clonal anergy , biology , clone (java method) , t cell receptor , clonal deletion , t cell , il 2 receptor , immunology , interleukin 2 , antigen , stimulation , microbiology and biotechnology , cytokine , immune system , gene , genetics , endocrinology
T‐cell anergy is a state of immunological tolerance characterized by unresponsiveness to antigenic stimulation. Previous studies have shown that anergy is induced in T cells following stimulation in the absence of adequate costimulatory signals. These cells fail to respond to stimulation via the T‐cell receptor (TCR), and fail to produce normal levels of interleukin‐2 (IL‐2). We present results here which show that low concentrations of the superantigen staphylococcal enterotoxin A (SEA) in the absence of antigen‐presenting cells induced both proliferation and anergy in the A.E7 T‐cell clone. Furthermore, under these conditions, the A.E7 clone remained responsive to exogenous IL‐2. Fluorescence‐activated cellular cytometry analysis revealed unaltered expression of the TCR/CD3 complex in the anergized clone; however, both CD4 and CD25 expression increased after 24 hr of stimulation by SEA under these conditions. Interestingly, a low level of IL‐2 production was measured during the induction of anergy. Most strikingly, stimulation of the A.E7 clone by SEA in combination with exogenous IL‐2 resulted in a more pronounced state of anergy. These results suggest that the induction of anergy is a process that is essentially independent of the production of IL‐2.