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CD4 TCRBV CDR3 Analysis in prevalent SLE Cases from two ethnic Groups

Center for Blood Research, Harvard Medical School, Kingston, Jamaica; Division of Rheumatology, Immunology and Allergy, Department of Medicine, Brigham and, Women's Hospital, Harvard Medical School, Kingston, Jamaica

L-Y Lu

Veterans General Hospital, Kaoshiung, Taiwan

K DeCeulaer

University Hospital, University of the West Indies, Mona Campus, Kingston, Jamaica

P H Schur

Division of Rheumatology, Immunology and Allergy, Department of Medicine, Brigham and, Women's Hospital, Harvard Medical School, Kingston, Jamaica

D Fici

Z Awdeh

W-Z Ding

E Levitan

Center for Blood Research, Harvard Medical School, Kingston, Jamaica

R Lew

Division of Rheumatology, Immunology and Allergy, Department of Medicine, Brigham and, Women's Hospital, Harvard Medical School, Kingston, Jamaica

G Uko

Center for Blood Research, Harvard Medical School, Kingston, Jamaica

C Gonzalez

Division of Rheumatology, Immunology and Allergy, Department of Medicine, Brigham and, Women's Hospital, Harvard Medical School, Kingston, Jamaica

We examined CD4+ T cell TCRBV-CDR3 transcripts from 19 lupus patients and 16 controls to test the hypothesis that CD4+ TCRBV-CDR3 expression in SLE differs from normals. Within the disease group we also performed exploratory analyses to determine the association between risk of oligoclonality and HLA-DRB specificities and the duration of the CDR3 patterns. Oligoclonal patterns consistent with CDR3 restriction were three times more likely in SLE than in controls (OR=3.7). TCRBV1, BV4, BV5.1, BV7, BV9, BV18 and BV22 gene segment CDR3 patterns of oligoclonality were seenexclusively amonglupus patients. HLA-DRB3increasedtherisk ofoligoclonalexpressionin SLE. In four patients studied over time, the pattern of TCRBV-CDR3 expression was stable in a second sample obtained 6–14 months later. The increased frequency of CD4+ T cell TCRBV-CDR3 oligoclonal expression in SLE when compared to controls and the persistence of these patterns are consistent with an expanded pool of autoreactive CD4 T cells in SLE which recognize peptides derived from autoantigens. The association of HLA-DRB3 genes with increased risk of CDR3 oligoclonality among the SLE subjects is compatible with the hypothesis that molecules encoded by HLA-DRB3 may facilitate autoantigen recognition by CD4 T cells.

Key Words: CD4+ Tcells • SLE • disease activity

Lupus, Vol. 8, No. 4, 311-319 (1999)
DOI: 10.1191/096120399678847902


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