MHC class I family proteins retard systemic lupus erythematosus autoimmunity and B cell lymphomagenesis.

Document Type

Article

Publication Date

11-1-2011

Keywords

Animals, B-Lymphocyte Subsets, CD4-Positive T-Lymphocytes, CD8-Positive T-Lymphocytes, H-2 Antigens, Histocompatibility Antigens Class I, Killer Cells, Natural, Lupus Erythematosus, Systemic, Lymphoma, B-Cell, Mice, Mice, Inbred Strains, Moloney murine leukemia virus, beta 2-Microglobulin

JAX Source

J Immunol 2011 Nov 1; 187(9):4695-704.

PMID

21964024

Volume

187

Issue

9

First Page

4695

Last Page

4704

ISSN

1550-6606

Abstract

Dysregulation of the T cell-dependent Ab response can lead to numerous immunological disorders, ranging from systemic lupus erythematosus to B cell lymphomas. Cellular processes governed by MHC class II proteins play a major role in this response and its dysregulation. The extent to which processes controlled by the diverse family of MHC class I proteins impact such autoimmune and neoplastic disorders, however, is less clear. In this study, we genetically dissect the contributions of individual MHC class I family members and the pathological processes under their control in the systemic lupus erythematosus-like disease of BXSB.Yaa mice and B cell lymphomagenesis of SJL mice. This study reveals a powerful repressive regulatory axis comprised of MHC class I-dependent CD8(+) T cells and NK cells. These results indicate that the predominant role of the MHC class I protein family in such immunological disorders is to protect from more aggressive diseases.

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