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Molecular mimicry has not been studied extensively in SLE, but a role for Th cells is well-established; it is clear that the expansion of autoreactive B cell requires pathogenic Th cells (8–11).However, the antigen specificity of the Th cells has been unclear.Matched sequences were more frequent within the mutated CDR3 repertoire and when sequences were derived from lupus mice with expanded anti-ds DNA B cells.Analyses of histone sequences showed that particular histone peptides were similar to VDJ junctions.We chose to compare heavy chain junctions (Ig VH CDR3 peptides) from mice with lupus with proteomes from microbes and mouse.The CDR3 of the heavy chain has the highest potential for novel peptides, both in terms of N region diversity (V–N1–D–N2–J) as well as the option of alternate reading frames of the D gene segment, and as a site for mutations.The following control data sets were downloaded from NCBI and compared to the IMGT/V-QUEST reference directory release: 201310-4 (14 March 2013) (36).Ig VH region family identification and clonality analysis were performed on the statistics module of IMGT/High V-QUEST.
The Norwegian Animal Research Authority approved the experiments.
The specificity of the Th cells that drive the expansion of anti-ds DNA B cells is unresolved.
However, anti-microbial, anti-histone, and anti-idiotype Th cell responses have been hypothesized to play a role.
We also found that mice suffering from Id-driven lupus (with high levels of anti-ds DNA responses) developed Th cell responses toward anti-ds DNA m Abs with CDR3 sequences that resembled histones, suggesting epitope spreading involving cationic peptide mimics including idiotypes and self proteins.
Mice were transgenic for both the λ2 MHC class II molecules (30, 31).