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Analysis of SLAM family receptors 2B4, CS1 and NTB-A in patients with Systemic Lupus Erythematosus (SLE) (49.22)

Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disease, characterized by the improper regulation of B lymphocytes that leads to the production of auto-antibodies. Several studies have identified a genetic susceptibility region called Sle 1 in mice and some human subjects. Re...

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Bibliographic Details
Published in:The Journal of immunology (1950) 2009-04, Vol.182 (1_Supplement), p.49-49.22
Main Authors: Mathew, Stephen O, Kim, Jong R, Pertusi, Raymond M, Patel, Rahul K, Mathew, Porunelloor A
Format: Article
Language:English
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Summary:Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disease, characterized by the improper regulation of B lymphocytes that leads to the production of auto-antibodies. Several studies have identified a genetic susceptibility region called Sle 1 in mice and some human subjects. Recently, genomic characterization of the Sle1b locus, identified a highly polymorphic cluster of genes coding for the signaling lymphocyte activation molecule (SLAM)-related receptors (SRRs). 2B4 (CD244), CS1 (CD319, CRACC) and NTB-A are members of SRRs and are expressed on NK, T, B cells and monocytes. The aim of this study was to investigate expression of members of the SRRs in peripheral blood mononuclear cells (PBMC) from patients with SLE. We analyzed PBMC from forty-six patients with SLE and thirty-one healthy individuals. The surface expressions of 2B4, CS1, and NTB-A on T cells, B cells, NK cells, and monocytes were analyzed by flow cytometry. 2B4 expression was upregulated on T cells but down-regulated on NK cells and monocytes in patients with SLE. B cells from patients with SLE significantly overexpressed CS1 compared to B cells from healthy controls. The surface expression of NTB-A was upregulated on T cells and monocytes, but down-regulated on B cells in patients with SLE. Our results suggest that altered expression of SRRs may be related to the abnormal B cell hyperactivity in patients with SLE. (Research supported by grants from Texas Higher Education Board and UNTHSC).
ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.182.Supp.49.22