NDLI: Cutting edge: in the absence of regulatory T cells, a unique Th cell population expands and leads to a loss of B cell anergy.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	De Santis, Jessica L. Leonardo, Steven M. Malherbe, Laurent P. Gauld, Stephen B.
Description	Country affiliation: United States Author Affiliation: Leonardo SM ( Division of Allergy/Immunology, Department of Pediatrics, Medical College of Wisconsin, Children's Research Institute, Milwaukee, WI 53226, USA.)
Abstract	The absence of regulatory T cells (Tregs) results in significant immune dysregulation that includes autoimmunity. The mechanism(s) by which Tregs suppress autoimmunity remains unclear. We have shown that B cell anergy, a major mechanism of B cell tolerance, is broken in the absence of Tregs. In this study, we identify a unique subpopulation of CD4(+) Th cells that are highly supportive of Ab production and promote loss of B cell anergy. Notably, this novel T cell subset was shown to express the germinal center Ag GL7 and message for the B cell survival factor BAFF, yet failed to express markers of the follicular Th cell lineage. We propose that the absence of Tregs results in the expansion of a unique nonfollicular Th subset of helper CD4(+) T cells that plays a pathogenic role in autoantibody production.
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	B-lymphocyte Subsets Immunology Cd4-positive T-lymphocytes Cell Differentiation Clonal Anergy Clonal Deletion T-lymphocytes, Regulatory Pathology Animals Cytology Metabolism Genetics Cell Lineage Cells, Cultured Coculture Techniques Mice Mice, Inbred C57bl 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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