The Science Journal of the Lander College of Arts and Sciences


David Schon


Autoimmune disease refers to a systemic immune response by the body against its own healthy tissue and cells. This results in various non-specific and systemic inflammatory processes that evolve into more than 100 individual diseases. Numerous biological similarities exist between the different pathophysiological pathways, including biochemical cascades and inflammasome mediators. This paper aims to investigate whether contracting one form of autoimmune disease can lead to the development of polyautoimmunity and multiple autoimmune syndrome. Scientists have identified chronic levels of high stress as a contributor to higher levels of C-reactive protein and several immune modulating interleukins, which can lead to both autoimmune and polyautoimmune processes (Steptoe et al., 2007). Immunologists and virologists have established how viruses can lead to autoreactive immune activity through molecular mimicry and epitope spreading. These same processes are found in all forms of inflammation and may explain the connection between undiagnosed adult-onset celiac disease and multiple autoimmune syndrome. Many genetic pathways have been identified as drivers of both individual autoimmune conditions and specific inflammasome mediators that could be responsible for familial based autoimmunity and specific subtypes of multiple autoimmune syndrome. Collectively, these studies underlie and illustrate a direct connection between several contributors that definitively link autoimmunity with polyautoimmunity.



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