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Signaling via CD28 costimulates lymphokine production, but does not reverse unresponsiveness to interleukin‐2 in anti‐CD3 triggered T h 1 cells
Author(s) -
Sommer Frank,
Röllinghoff Martin,
Lohoff Michael
Publication year - 1993
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.1830231018
Subject(s) - lymphokine , biology , cd28 , interleukin 2 , microbiology and biotechnology , cd3 , immunology , t cell , cytokine , immune system , cd8
Abstract Previously, it has been described that the ability of murine T h 1 cells to proliferate in response to exogenous interleukin (IL)‐2 is blocked when these cells are exposed to immobilized anti‐CD3 antibodies. In the present study we examined whether simultaneous triggering of the T cell antigen CD28 can prevent the induction of unresponsiveness to IL‐2 in T h 1 cells. We report that costimulation of T h 1 cells with anti‐CD28 monoclonal antibodies (mAb) did not overcome unresponsiveness to IL‐2 induced by various amounts of immobilized anti‐CD3 antibodies. However, stimulation with anti‐CD28 mAb strongly augmented IL‐2 and interferon‐γ production in anti‐CD3‐exposed T h 1 cells. Thus, despite the fact that anti‐CD28 mAb is a potent costimulus for lymphokine production, signaling through CD28 does not seem to be sufficient to trigger proliferation in T h 1 cells activated via the T cell receptor. These data suggest the existence of at least three signals to trigger T h 1 cell activation. The first is mediated by ligation of the T cell receptor. One cosignal, delivered by the CD28 molecule, leads to IL‐2 production. A third, still undefined, signal is required for proliferation in response to IL‐2.