Autoimmune disease: why and where it occurs

By P. Marrack, J. Kappler, B. Kotzin. Nature Medicine, 2001

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Synovial fibroblasts: key players in rheumatoid arthritis. (2006, background): “RA is a systemic disorder, and it is commonly accepted that it emerges from a variable combination of individual genetic predisposition, environmental factors (such as potential but unproven infectious agents) and dysregulated immune responses [2–5].”
A Proposed Classification of the Immunological Diseases (2006, background): “]; this hypothesis is closely allied with the proposed generic definition of autoinflammation. Looking at immunological disease from the autoimmunity perspective, several groups have drawn attention to the possible role of tissue-specific factors in autoimmunity [”
A missense single-nucleotide polymorphism in a gene encoding a protein tyrosine phosphatase (PTPN22) is associated with rheumatoid arthritis. (2004, unknown): “…the minor allele of the PTPN22 SNP reported here is also associated with T1D (Bottini et al. 2004) supports the hypothesis that there are common genetic variants that contribute to general immune dysregulation and susceptibility to autoimmunity (Marrack et al. 2001; Wandstrat and Wakeland 2001).”
IL-6 in inflammation, autoimmunity and cancer (2020, background): “Instead, hyper-activation of the immune system to the target tissue may be a consequent event that is initiated by local initiators in non-immune target tissue in a manner dependent on genetic and/or environmental factors (1, 47, 48, 50).”