Over the past 25 years, much has been learned about the cellular and humoral immune-mediated mechanisms involved in the pathogenesis of DM. More recently, the role of complement, specifically the MAC, in immune-mediated vascular injury has been further elucidated. Additionally, susceptibility to develop juvenile DM has been linked with the class II major histocompatibility complex HLA-DQA1*0501 allele, and disease course and various complications have been associated with polymorphisms at the TNF-α-308 locus. In this way, the genetic background of children with DM is integrally entwined with the type of elicited inflammatory response. More recently, data has become available regarding the molecular genetics of children affected with juvenile DM and the impact these genes have on disease expression and clinical course [1].
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(2009). Pathogenesis of Dermatomyositis. In: Dermatomyositis. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-79313-7_37
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