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 explorator
y analyses to determine the association between risk of oligoclonality and
HLA-DRB specificities and the duration of the CDR3 patterns. Oligoclonal pa
tterns 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 g
ene segment CDR3 patterns of oligoclonality were seen exclusively among lup
us patients. HLA-DRB3 increased the risk of oligoclonal expression in SLE.
In four patients studied over time, the pattern of TCRBV-CDR3 expression wa
s stable in a second sample obtained 6-14 months later. The increased frequ
ency of CD4 + T cell TCRBV-CDR3 oligoclonal expression in SLE when compared
to controls and the persistence of these patterns are consistent with an e
xpanded pool of autoreactive CD4 T cells in SLE which recognize peptides de
rived from autoantigens. The association of HLA-DRB3 genes with increased r
isk of CDR3 oligoclonality among the SLE subjects is compatible with the hy
pothesis that molecules encoded by HLA-DRB3 may facilitate autoantigen reco
gnition by CD4 T cells.