NDLI: Breakdown in repression of IFN-Î³ mRNA leads to accumulation of self-reactive effector CD8+ T cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Cho, Jae-Ho Lee, Sau K. Davey, Gayle Karupiah, Guna Duan, Guowen Bertram, Edward M. Chang, Pheh-Ping Sprent, Jonathan Heath, William R. Hu, Xin Vinuesa, Carola G.
Description	Country affiliation: Australia Author Affiliation: Chang PP ( Department of Pathogens and Immunity, John Curtin School of Medical Research, Australian National University, Canberra, Australia.)
Abstract	Tight regulation of virus-induced cytotoxic effector CD8(+) T cells is essential to prevent immunopathology. Naturally occurring effector CD8(+) T cells, with a KLRG1(hi) CD62L(lo) phenotype typical of short-lived effector CD8(+) T cells (SLECs), can be found in increased numbers in autoimmune-prone mice, most notably in mice homozygous for the san allele of Roquin. These SLEC-like cells were able to trigger autoimmune diabetes in a susceptible background. When Roquin is mutated (Roquin(san)), effector CD8(+) T cells accumulate in a cell-autonomous manner, most prominently as SLEC-like effectors. Excessive IFN-Î³ promotes the accumulation of SLEC-like cells, increases their T-bet expression, and enhances their granzyme B production in vivo. We show that overexpression of IFN-Î³ was caused by failed posttranscriptional repression of Ifng mRNA. This study identifies a novel mechanism that prevents accumulation of self-reactive cytotoxic effectors, highlighting the importance of regulating Ifng mRNA stability to maintain CD8(+) T cell homeostasis and prevent CD8-mediated autoimmunity.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	2
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-07-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cd8-positive T-lymphocytes Immunology Cell Aggregation Cytotoxicity, Immunologic Down-regulation Interferon-gamma Antagonists & Inhibitors Genetics Rna, Messenger Adoptive Transfer Animals Pathology Transplantation Cell Aging Homeostasis Immunosuppressive Agents Metabolism Biosynthesis Lectins, C-type Mice Mice, Inbred C57bl Mice, Knockout Mice, Transgenic Mutation Rna Stability Trans-activators Ubiquitin-protein Ligases Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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