Cutting edge: in the absence of regulatory T cells, a unique Th cell population expands and leads to a loss of B cell anergy. J Immunol 2012 Jun 01;188(11):5223-6
Date
05/01/2012Pubmed ID
22544930DOI
10.4049/jimmunol.1103731Scopus ID
2-s2.0-84862058052 (requires institutional sign-in at Scopus site) 13 CitationsAbstract
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.
Author List
Leonardo SM, De Santis JL, Malherbe LP, Gauld SBAuthor
Jessica L. De Santis PhD, MA, BS Assistant Professor in the Anesthesiology department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsB-Lymphocyte Subsets
CD4-Positive T-Lymphocytes
Cell Differentiation
Cell Lineage
Cells, Cultured
Clonal Anergy
Clonal Deletion
Coculture Techniques
Mice
Mice, Inbred C57BL
Mice, Transgenic
T-Lymphocytes, Regulatory
