title: The role of innate immune pathways in type 1 diabetes pathogenesis.
abstract: OBJECTIVE
  Type 1 diabetes (T1D) is an autoimmune disease typically believed to result from malfunctions in adaptive immune response signaling which result in activation of self-reactive T cells. However, recent research has indicated components of the innate immune response as having a key role in the initiation of the autoimmune process of T1D. This review will highlight recent studies which examined the role of innate immune response signaling and the connections to T1D pathogenesis.
  
  
  RESULTS
  Investigations indicate that components of innate immunity, including inflammation and Toll-like receptor signaling, are involved in pancreatic islet infiltration and insulitis. Recent studies examining the role of viral infections in T1D development also implicate innate immune response signaling in disease pathogenesis.
  
  
  CONCLUSIONS
  Current research indicates that components of innate immune response signaling are involved in the initiation of the autoimmune process which results in the eventual destruction of beta cells during T1D pathogenesis. Continuing efforts by researchers to uncover the molecular pathways of innate immunity linked to T1D development could potentially lead to therapeutics capable of preventing and curing the autoimmune disease.
authors.affiliation: Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA.
authors.forename: Steven C
authors.initials: SC
authors.lastname: Pino
authors.forename: Annie J
authors.initials: AJ
authors.lastname: Kruger
authors.forename: Rita
authors.initials: R
authors.lastname: Bortell
mesh_terms: D000818:Animals; D003922:Diabetes Mellitus, Type 1 / Q000209:etiology* / Q000276:immunology; D006801:Humans; D007113:Immunity, Innate / Q000502:physiology*; D007249:Inflammation / Q000276:immunology; D015398:Signal Transduction / Q000276:immunology / Q000502:physiology*; D051193:Toll-Like Receptors / Q000502:physiology; D014777:Virus Diseases / Q000209:etiology / Q000276:immunology
chemical_list: D051193:Toll-Like Receptors