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Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: https://hdl.handle.net/2445/209200
Role Of The Innate Immunity In The Etiopathogenesis of Primary Sjögren Syndrome: Influence Of Viral And Immunogenetic Factors Related To Cell Adhesion Molecules In Systemic Disease And Autoantibody Profile
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[eng] Sjögren Syndrome is a systemic autoimmune disease that affects the exocrine glands, most notably the salivary and lacrimal glands, although it can affect other mucosal surfaces. Inflammation at these sites leads to a spectrum of sicca symptoms, thereby the predominantly symptoms are dryness of the mouth and the eyes. It is not limited to exocrine gland dysfunction; it may involve any other extraglandular systems as well (kidneys, lungs, central and peripheral nervous systems, among others). It is called primary SjS when it exists as an isolated diagnosis, and associated SjS when it co-occurs with another systemic autoimmune disorder. It is characterized by the presence of anti-Ro/La antibodies and/or the presence of focal lymphocytic sialadenitis. SjS is a chronic, systemic autoimmune disease for which no cure currently exists and the management should be organ-specific. The etiopathogenetic factors contributing to SjS remain enigmatic. The development of SjS can be considered as occurring in three stages: 1) an environmental trigger incites autoimmunity against a specific genetic background, b) the autoimmune response becomes chronic due to aberrant regulatory mechanisms within the immune system, and c) lymphoepithelial lesions and subsequent tissue damage arise from persistent inflammation. The prevailing theory, termed 'autoimmune epithelitis,' posits that the epithelial cells of the exocrine glands are the primary sites of inflammation in SjS. According to this model, lymphocytic infiltrates develop in epithelial cells surrounding or invading organs. These epithelial cells act as central players in the autoimmune response by functioning as atypical antigen-presenting cells. Extensive research has been devoted to investigating the role of salivary gland epithelial cells and epithelial cells of the lacrimal glands in SjS. These studies have demonstrated that epithelial cells are capable of orchestrating both innate and acquired immune responses, thereby affirming their crucial role in the disease process. The study of innate immunity in the context of autoimmune diseases like SjS is still in its infancy. Emerging evidence suggests that innate immune components may play a critical role in SjS etiopathogenesis. In this thesis, we focus on the role of HCV and innate immunity components (pattern recognition receptor SP-D, scavenger receptors CD5 and CD6 and adhesion molecule ALCAM) in SjS etiopathogenesis. Individuals infected with HCV often present sicca symptoms that mimic those of SjS. The virus is known to be associated with autoimmune phenomena and histopathological evidence shows that HCV can be isolated in the salivary glands of infected individuals. SP-D is found in epithelial cells and luminar material in glandular tissues, potentially implicating it in the pathogenesis of primary SjS. CD5, CD6, and ALCAM/CD166 are expressed in inflamed tissues of SjS, and their SNPs have been linked to other immune-mediated inflammatory diseases. Based on the evidence, we believe that individuals with HCV infection and those with specific SNPs in innate immunity components (SP-D, CD5/CD6, and ALCAM/CD166) may exhibit altered disease expression and immunological profiles in SjS. Understanding the role of these factors could provide critical insights into the onset and perpetuation of autoimmune responses in SjS. The overarching goal is to advance our understanding of how innate immunity machinery and specific etiopathogenic factors contribute to the complex landscape of SjS, thereby providing new avenues for diagnosis, prognosis, and therapeutic intervention.
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GHEITASI, Hoda. Role Of The Innate Immunity In The Etiopathogenesis of Primary Sjögren Syndrome: Influence Of Viral And Immunogenetic Factors Related To Cell Adhesion Molecules In Systemic Disease And Autoantibody Profile. [consulta: 12 de desembre de 2025]. [Disponible a: https://hdl.handle.net/2445/209200]