The lupusTCR-alpha chains probably contact the nucleosomal peptide complexed with MHC with relatively high affinity/avidity to sustain TCR signaling, because CD4 coreceptor was not required for promiscuous recognition.
The analysis of the beta chain of the TCR revealed little clonotypic T cell expansion in the peripheral blood of lupus patients in remission, whereas in patients with active disease many dominant T cell clonal expansions without any distinct V beta bias were observed.
Mixed connective tissue disease (MCTD) and systemic lupus erythematosus (SLE) are autoimmune diseases with a genetic background, and it is reasonable to suggest that aberrations in T cell receptor (TCR) genes could contribute to these diseases, as they play an important role in immune regulation.
To test the possibility that T cell antigen receptor (TcR) genes are linked to the genes involved in the pathogenesis of systemic lupus erythematosus (SLE), genomic DNA restriction fragment length polymorphisms were studied, using the Southern blot technique, in 5 families with multiple members with SLE, 14 unrelated SLE patients, and 14 normal controls.