Cellular stress and innate inflammation in organ-specific autoimmunity: lessons learned from vitiligo
Department of Medicine, Division of Dermatology; UMass Metabolic Network
Cell Biology | Cellular and Molecular Physiology | Immune System Diseases | Immunity
For decades, research in autoimmunity has focused primarily on immune contributions to disease. Yet recent studies report elevated levels of reactive oxygen species and abnormal activation of the unfolded protein response in cells targeted by autoimmunity, implicating cellular stress originating from the target tissue as a contributing factor. A better understanding of this contribution may help to answer important lingering questions in organ-specific autoimmunity, as to what factors initiate disease and what directs its tissue specificity. Vitiligo, an autoimmune disease of the skin, has been the focus of translational research for over 30 years, and both melanocyte stress and immune mechanisms have been thought to be mutually exclusive explanations for pathogenesis. Chemical-induced vitiligo is a unique clinical presentation that reflects the importance of environmental influences on autoimmunity, provides insight into a new paradigm linking cell stress to the immune response, and serves as a template for other autoimmune diseases. In this review, I will discuss the evidence for cell stress contributions to a number of autoimmune diseases, the questions that remain, and how vitiligo, an underappreciated example of organ-specific autoimmunity, helps to answer them.
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Citation: Immunol Rev. 2016 Jan;269(1):11-25. doi: 10.1111/imr.12369. Link to article on publisher's site
Harris, John E., "Cellular stress and innate inflammation in organ-specific autoimmunity: lessons learned from vitiligo" (2016). UMass Metabolic Network Publications. 60.