Autoimmune gld mutation uncouples suicide and cytokine/proliferation pathways in activated, mature T cells
- 1 September 1993
- journal article
- research article
- Published by Wiley in European Journal of Immunology
- Vol. 23 (9) , 2379-2382
- https://doi.org/10.1002/eji.1830230951
Abstract
Antigen receptor-directed suicide plays an important role in the elimination of potentially autoaggressive immature T cells during thymic differentiation. Here we demonstrate evidence for a second pathway of receptor-directed suicide in mature T cells that is missing in a mutant strain (gld) of mice with an “autoimmune” lymphoproliferative syndrome. The defect is evident within the gld activated T cell and does not require the presence of an antigen-presenting cell for its expression. Receptor-driven suicide is intact in immature T cells of animals with this mutation. These results support the significance of receptor-directed suicide in the mature T cell compartment and suggest that the immune system may use three independent pathways for regulating programmed cell death in shaping and controlling the immune response.Keywords
This publication has 28 references indexed in Scilit:
- Sensitivity of T cells to anti‐CD3‐stimulated suicide is independent of functional phenotypeEuropean Journal of Immunology, 1992
- Lymphoproliferation disorder in mice explained by defects in Fas antigen that mediates apoptosisNature, 1992
- bcl-2 inhibits multiple forms of apoptosis but not negative selection in thymocytesCell, 1991
- lnterleukin-2 programs mouse αβ T lymphocytes for apoptosisNature, 1991
- The polypeptide encoded by the cDNA for human cell surface antigen Fas can mediate apoptosisCell, 1991
- Superantigens: Mechanism of T-Cell Stimulation and Role in Immune ResponsesAnnual Review of Immunology, 1991
- Lpr and gld: Single Gene Models of Systemic Autoimmunity and Lymphoproliferative DiseaseAnnual Review of Immunology, 1991
- Differences defined by bone marrow transplantation suggest that lpr and gld are mutations of genes encoding an interacting pair of molecules.The Journal of Experimental Medicine, 1990
- A new allele of the lpr locus, lprcg, that complements the gld gene in induction of lymphadenopathy in the mouse.The Journal of Experimental Medicine, 1990
- Deletion of potentially self-reactive T cell receptor specificities in L3T4-, Lyt-2- T cells of lpr mice.The Journal of Experimental Medicine, 1988