NDLI: IL-21 promotes lupus-like disease in chronic graft-versus-host disease through both CD4 T cell- and B cell-intrinsic mechanisms.

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IL-21 promotes lupus-like disease in chronic graft-versus-host disease through both CD4 T cell- and B cell-intrinsic mechanisms.

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B cell tolerance and positive selection in $lupus^{}$

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IL-21 promotes lupus-like disease in chronic graft-versus-host disease through both CD4 T cell- and B cell-intrinsic mechanisms.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Luzina, Irina Rus, Violeta Chen, Ching Nguyen, Vinh Tegla, Cosmin Rus, Horea
Description	Country affiliation: United States Author Affiliation: Nguyen V ( Department of Medicine, University of Maryland School of Medicine, Baltimore, MD, USA.)
Abstract	T cell-driven B cell hyperactivity plays an essential role in driving autoimmune disease development in systemic lupus erythematosus. IL-21 is a member of the type I cytokine family with pleiotropic activities. It regulates B cell differentiation and function, promotes T follicular helper (T(FH)) cell and Th17 cell differentiation, and downregulates the induction of T regulatory cells. Although IL-21 has been implicated in systemic lupus erythematosus, the relative importance of IL-21R signaling in CD4(+) T cells versus B cells is not clear. To address this question, we took advantage of two induced models of lupus-like chronic graft-versus-host disease by using wild-type or IL-21R(-/-) mice as donors in the parent-into-F1 model and as hosts in the Bm12â B6 model. We show that IL-21R expression on donor CD4(+) T cells is essential for sustaining T(FH) cell number and subsequent help for B cells, resulting in autoantibody production and more severe lupus-like renal disease, but it does not alter the balance of Th17 cells and regulatory T cells. In contrast, IL-21R signaling on B cells is critical for the induction and maintenance of germinal centers, plasma cell differentiation, autoantibody production, and the development of renal disease. These results demonstrate that IL-21 promotes autoimmunity in chronic graft-versus-host disease through both CD4(+) T cell- and B cell-intrinsic mechanisms and suggest that IL-21 blockade may attenuate B cell hyperactivity, as well as the aberrant T(FH) cell pathway that contributes to lupus pathogenesis.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1200318
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	B-lymphocyte Subsets Immunology Cd4-positive T-lymphocytes Graft Vs Host Disease Interleukin-21 Receptor Alpha Subunit Physiology Interleukins Lupus Erythematosus, Systemic Animals Pathology Cell Differentiation Genetics Chronic Disease Down-regulation Complications Biosynthesis Deficiency Etiology Lymphocyte Cooperation Mice Mice, Inbred C57bl Mice, Knockout Mice, Transgenic T-lymphocytes, Regulatory Th17 Cells Up-regulation 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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