Retinoic acid‐inducible gene (RIG)‐I‐like receptors (RLR), including melanoma differentiation‐associated protein 5 (MDA5) and RIG‐I, recognize the double‐strand (ds) virus RNA and induce the production of Type I interferon (Type I IFN) and pro‐inflammatory cytokines,
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which are associated with autoimmune diseases, such as systemic Lupus erythematodes (SLE) and Dermatomyositis. After binding to the viral dsRNA, N‐terminal caspase activation and recruitment domains (CARDs) of RLR interact with mitochondrial antiviral‐signalling protein (MAVS) and eventually, prion‐like aggregates are formed. These aggregates activate transcription factor NF‐ĸB, which in turn stimulates the production of Type I IFN, interleukin‐6 (IL‐6) and further pro‐inflammatory cytokines.
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Activation of plasmacytoid dendritic cells (pDC) follows Type I IFN‐mediated activation of B cells which can lead to autoantibody production, e.g, anti‐MDA5 antibodies.