IL-2 protects against anti-CD3-induced cell death in human medullary thymocytes.
Open Access
- 1 September 1990
- journal article
- research article
- Published by Oxford University Press (OUP) in The Journal of Immunology
- Vol. 145 (5) , 1364-1368
- https://doi.org/10.4049/jimmunol.145.5.1364
Abstract
In recent years, several studies have confirmed the clonal elimination of thymocytes with receptors that recognize Ag and MHC molecules present on the membrane of thymic stromal cells, a process that may be relevant to the establishment of self-tolerance. In our work, we show that anti-CD3 treatment of single positive CD4+ or CD8+ human medullary thymocytes (obtained by anti-CD1a plus C) induces their apoptotic death. Some events commonly associated with the early steps of normal activation (IL-2R expression, increase in cytoplasmic Ca2+) are also induced after anti-CD3 treatment. Nevertheless, IL-2 is not secreted by these activated cells. The addition of exogenous IL-2 inhibits the apoptosis induced by anti-CD3. We suggest that the lack of secretion of IL-2 by medullary thymocytes may be a physiologic mechanism implicated in the process of negative selection that leads to tolerance.This publication has 4 references indexed in Scilit:
- Macrophages phagocytose thymic lymphocytes with productively rearranged T cell receptor alpha and beta genes.The Journal of Experimental Medicine, 1988
- The effect of thymus environment on T cell development and toleranceCell, 1988
- Selective inhibition of interleukin 2 gene function following thymocyte antigen/major histocompatibility complex receptor crosslinking: possible thymic selection mechanism.Proceedings of the National Academy of Sciences, 1987
- A rapid, large scale purification procedure for gibbon interleukin 2.The Journal of Immunology, 1983