NDLI: IL-10+ CTLA-4+ Th2 inhibitory cells form in a Foxp3-independent, IL-2-dependent manner from Th2 effectors during chronic inflammation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Goodnow, Chris C. Altin, John A. Cook, Matthew C.
Description	Country affiliation: Australia Author Affiliation: Altin JA ( Department of Immunology, John Curtin School of Medical Research, Australian National University, Canberra, Australian Capital Territory 0200, Australia.)
Abstract	Activated Th cells influence other T cells via positive feedback circuits that expand and polarize particular types of response, but little is known about how they may also initiate negative feedback against immunopathological reactions. In this study, we demonstrate the emergence, during chronic inflammation, of GATA-3(+) Th2 inhibitory (Th2i) cells that express high levels of inhibitory proteins including IL-10, CTLA-4, and granzyme B, but do so independently of Foxp3. Whereas other Th2 effectors promote proliferation and IL-4 production by naive T cells, Th2i cells suppress proliferation and IL-4 production. We show that Th2i cells develop directly from Th2 effectors, in a manner that can be promoted by effector cytokines including IL-2, IL-10, and IL-21 ex vivo and that requires T cell activation through CD28, Card11, and IL-2 in vivo. Formation of Th2i cells may act as an inbuilt activation-induced feedback inhibition mechanism against excessive or chronic Th2 responses.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	11
Volume Number	188
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-06-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Ctla-4 Antigen Biosynthesis Forkhead Transcription Factors Inflammation Mediators Physiology Interleukin-10 Interleukin-2 Th2 Cells Immunology Animals Deficiency Cell Differentiation Genetics Cells, Cultured Chronic Disease Granzymes Immune Tolerance Inflammation Metabolism Pathology Mice Mice, Inbred C57bl Mice, Knockout Mice, Transgenic Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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