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dc.contributor.authorPino, Steven C.
dc.contributor.authorKruger, Annie J.
dc.contributor.authorBortell, Rita
dc.date2022-08-11T08:08:47.000
dc.date.accessioned2022-08-23T16:08:17Z
dc.date.available2022-08-23T16:08:17Z
dc.date.issued2010-04-01
dc.date.submitted2010-05-08
dc.identifier.issn1752-2978
dc.identifier.pmid20125005
dc.identifier.urihttp://hdl.handle.net/20.500.14038/32412
dc.description.abstractPURPOSE OF REVIEW: 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. RECENT FINDINGS: 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. SUMMARY: 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.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=20125005&dopt=Abstract">Link to article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1097/MED.0b013e3283372819
dc.rightsCitation: Current Opinion in Endocrinology, Diabetes and Obesity 2010 Apr;17(2):126-30.
dc.subjectDiabetes Mellitus, Type 1
dc.subjectImmunity, Innate
dc.subjectLaboratory and Basic Science Research
dc.subjectMedicine and Health Sciences
dc.titleThe role of innate immune pathways in type 1 diabetes pathogenesis.
dc.typeJournal Article
dc.source.journaltitleCurr Opin Endocrinol Diabetes Obes
dc.source.volume17
dc.source.issue2
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_mdphd/12
dc.identifier.contextkey1303055
html.description.abstract<p>PURPOSE OF REVIEW: 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.</p> <p>RECENT FINDINGS: 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.</p> <p>SUMMARY: 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.</p>
dc.identifier.submissionpathgsbs_mdphd/12
dc.contributor.departmentGraduate School of Biomedical Sciences, MD/PhD Program
dc.contributor.departmentDepartment of Medicine, Division of Diabetes
dc.contributor.studentAnnie J. Kruger


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