Signaling via CD28 costimulates lymphokine production, but does not reverse unresponsiveness to interleukin-2 in anti-CD3 triggered Th1 cells
✍ Scribed by Frank Sommer; Martin Röllinghoff; Michael Lohoff
- Book ID
- 102163459
- Publisher
- John Wiley and Sons
- Year
- 1993
- Tongue
- English
- Weight
- 485 KB
- Volume
- 23
- Category
- Article
- ISSN
- 0014-2980
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✦ Synopsis
Signaling via CD28 costimulates lymphokine production, but does not reverse unresponsiveness to interleukin-2 in anti-CD3 triggered T h l cells* Mikrobiologie, Universitat Erlangen-Nurnberg, Erlangen
Previously, it has been described that the ability of murineTh1 cells to proliferate in response to exogenous interleukin (1L)-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 inThl cells. We report that costimulation of T h l 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-y production in anti-CD3-exposed Thl 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 l cells activated via theT cell receptor.These data suggest the existence of at least three signals to trigger T h l cell activation.The first is mediated by ligation of theT 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.