Polymorphisms in the human complement C4 genes

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Early studies showed that AIH-1 was frequently associated with persistently low serum complement levels. C4 phenotyping revealed an association of null allotypes at the C4A or the C4B loci with AIH-1 and lower serum C4 levels in patients with C4A [16]. Furthermore, C4A deletions are associated with increased mortality and a higher tendency to relapse during immunosuppressive treatment. Homozygosity for C4A deletion correlated with a much stronger increase in the relative risk (RR) for hepatitis (RR = 18.1) than did a single deletion (RR = 3.3) [16]. While the increased risk for AIH-1 in patients with a single gene deletion may be the result of a strong linkage disequilibrium with HLA B3*0101, the strong increase in risk in homozygous patients suggests an additional role for C4 in disease susceptibility.

Figure 23.2 Structure of the peptide-binding groove of HLA-DR.

The position of residues that confer increased risk for different autoimmune diseases is shown. Abbreviations: autoimmune hepatitis (AIH): insulin-dependent diabetes mellitus (IDDM); major histocompatibility complex (MHC); primary biliary cirrhosis (PBC): primary sclerosing cholangitis (PSC); rheumatoid arthritis (RA).

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Figure 23.2 Structure of the peptide-binding groove of HLA-DR.

The position of residues that confer increased risk for different autoimmune diseases is shown. Abbreviations: autoimmune hepatitis (AIH): insulin-dependent diabetes mellitus (IDDM); major histocompatibility complex (MHC); primary biliary cirrhosis (PBC): primary sclerosing cholangitis (PSC); rheumatoid arthritis (RA).

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