PubMed · 10635770
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S Takemura. 1999. [The second component of complement, C2].. https://pubmed.ncbi.nlm.nih.gov/10635770/
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Previous research and therapy in renal transplantation largely focused on the cellular arm of the adaptive immune response. Evidence is emerging that innate immune mechanisms, particularly complement, play a greater role in inflammatory and immune responses against the graft than has been previously recognized. Alternative complement pathway activation appears to mediate renal ischaemia/reperfusion injury, and proximal tubular cells may be both the source and the site of attack of complement components in this setting. Locally produced complement also plays a role in the development of both cellular and antibody-mediated immune responses against the graft. C4d staining has emerged as a useful marker of humoral rejection both in the acute and in the chronic setting and led to renewed interest in the significance of anti-donor antibody formation. A number of therapies are in development which inhibit complement or reduce local synthesis, and may lead to an improved clinical outcome following renal transplantation.
A variable endogenous retroviral element has been identified in intron 9 of the complement C4 gene [HERV-K(C4)], which maps to the class III region of the major histocompatibility complex (MHC) on chromosome 6p21.3. Genetic susceptibility to type I diabetes is mainly conferred by the MHC locus and the complement C4 region has been implied to contribute to human leukocyte antigen DQ (HLA-DQ) mediated disease risk. As the HERV-K(C4) insertion has been suggested to modulate expression of homologous genes, we investigated its transmission in 220 families with an offspring affected by type I diabetes as a potential disease susceptibility marker. There was no preferential transmission of the HERV-K(C4) insertion to affected offspring (P(TDT) = 0.79). Although 77.7% of HLA-DQ8 carried the HERV-K(C4) insertion, only 52.9% of -DQ2 haplotypes did (P(chi(2)) < 0.01). However, its insertion or deletion did not modulate the risk conferred by HLA-DQ8 (DQA1*0301-DQB1*0302) (P(chi(2)) = 0.27) or -DQ2 (DQA1*0501-DQB1*0201) (P(chi(2)) = 0.46). Thus, the HERV-K(C4) insertion is not associated with type I diabetes in Germans.
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