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The Journal of Immunology, Vol 156, Issue 8 2769-2775, Copyright © 1996 by American Association of Immunologists
ARTICLES |
G Lombardi, R Hargreaves, S Sidhu, N Imami, L Lightstone, S Fuller-Espie, M Ritter, P Robinson, A Tarnok and R Lechler
Department of Immunology, Royal Postgraduate Medical School, London, United Kingdom.
Conflicting results of the effects of Ag presentation by MHC class II- expressing T cells have been described. In some studies class II- expressing T cells have been shown to act as effective APCs, while others have reported that the recognition of Ag on the surface of another T cell inactivates IL-2 production. In this study we have investigated the mechanisms involved in Ag presentation by T cells. The results obtained suggest that 1) lack of costimulation is not responsible for the inhibitory effects of T cell Ag presentation on IL- 2 production; the provision of costimulation by immobilized anti-CD28 Ab or by the addition of accessory cells failed to reverse the effects of T cell Ag presentation, but restored the response to immobilized anti-CD3; 2) T cell Ag presentation induced a minimal increase in intracellular Ca2+ compared with that induced by antigen-pulsed B cells; this difference in the calcium response is not explained by quantitative differences in ligand density between B cells and T cells; and 3) despite the weak calcium signal, T cell presentation supported IL-4 release in the absence of IL-2 production. Taken together these data suggest that T cell Ag presentation leads to altered TCR/CD3- transduced signals, which biases the T cell towards a Th2 phenotype.
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