WITHIN THE last 10 years, an immunologic phenomenon termed epitope spreading has been increasingly recognized as an important pathogenic mechanism responsible for the initiation and/or progression of autoimmune diseases.1,2Epitope spreading could be defined as a specific autoreactive lymphocyte (T- or B-cell) response to endogenous epitopes, which are distinct from and non–cross-reactive with the disease-inducing epitopes, on the (same or different) proteins secondary to the release of such a self-protein during an autoimmune response.2,3 Similarly, a specific primary autoreactive lymphocyte response to endogenous epitopes can arise from an inflammatory injury that releases the involved epitopes.2,3 In other words, an autoimmune or inflammatory disease process can cause tissue damage such that certain protein tissue components originally hidden from the autoreactive T or B cells become exposed and evoke a secondary or primary autoimmune response, respectively (Figure 1).2,3
Chan LS. Epitope Spreading in Paraneoplastic Pemphigus: Autoimmune Induction in Antibody-Mediated Blistering Skin Diseases. Arch Dermatol. 2000;136(5):663–664. doi:10.1001/archderm.136.5.663
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