NDLI: B7-CD28 costimulatory signals control the survival and proliferation of murine and human Î³Î´ T cells via IL-2 production.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Mancio-Silva, Liliana Ribot, Julie C. Debarros, Ana Pamplona, Ana Silva-Santos, Bruno
Description	Country affiliation: Portugal Author Affiliation: Ribot JC ( Unidade de Imunologia Molecular, Instituto de Medicina Molecular, Faculdade de Medicina, Universidade de Lisboa, 1649-028 Lisboa, Portugal. jribot@fm.ul.pt)
Abstract	Î³Î´ T cells play key nonredundant roles in immunity to infections and tumors. Thus, it is critical to understand the molecular mechanisms responsible for Î³Î´ T cell activation and expansion in vivo. In striking contrast to their ß counterparts, the costimulation requirements of Î³Î´ T cells remain poorly understood. Having previously described a role for the TNFR superfamily member CD27, we since screened for other nonredundant costimulatory receptors in Î³Î´ T cell activation. We report in this article that the Ig superfamily receptor CD28 (but not its related protein ICOS) is expressed on freshly isolated lymphoid Î³Î´ T cells and synergizes with the TCR to induce autocrine IL-2 production that promotes Î³Î´ cell survival and proliferation in both mice and humans. Specific gain-of-function and loss-of-function experiments demonstrated a nonredundant function for CD28 interactions with its B7 ligands, B7.1 (CD80) and B7.2 (CD86), both in vitro and in vivo. Thus, Î³Î´ cell proliferation was significantly enhanced by CD28 receptor agonists but abrogated by B7 Ab-mediated blockade. Furthermore, Î³Î´ cell expansion following Plasmodium infection was severely impaired in mice genetically deficient for CD28. This resulted in the failure to mount both IFN-Î³-mediated and IL-17-mediated Î³Î´ cell responses, which contrasted with the selective effect of CD27 on IFN-Î³-producing Î³Î´ cells. Our data collectively show that CD28 signals are required for IL-2-mediated survival and proliferation of both CD27(+) and CD27(-) Î³Î´ T cell subsets, thus providing new mechanistic insight for their modulation in disease models.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	3
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Antigens, Cd28 Physiology B7 Antigens Cell Proliferation Interleukin-2 Biosynthesis Receptors, Antigen, T-cell, Gamma-delta Signal Transduction Immunology T-lymphocyte Subsets Animals Cell Survival Cells, Cultured Malaria, Falciparum Metabolism Pathology Mice Mice, Inbred C57bl Mice, Knockout Plasmodium Falciparum Parasitology Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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