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Toll-like receptor 3 is critical for coxsackievirus B4-induced type 1 diabetes in female NOD mice.
McCall, Kelly D; Thuma, Jean R; Courreges, Maria C; Benencia, Fabian; James, Calvin B L; Malgor, Ramiro; Kantake, Noriko; Mudd, William; Denlinger, Nathan; Nolan, Bret; Wen, Li; Schwartz, Frank L.
Afiliación
  • McCall KD; Departments of Specialty Medicine (K.D.M., M.C.C., W.M., N.D., B.N., F.L.S.) and Biomedical Sciences (K.D.M., F.B., C.B.L.J., R.M., N.K.) and Diabetes Institute (K.D.M., J.R.T., M.C.C., R.M., W.M., N.D., B.N., F.L.S.), Ohio University Heritage College of Osteopathic Medicine, Athens, Ohio 45701; Department of Biological Sciences (K.D.M.) and Molecular and Cellular Biology Program (K.D.M., F.B., C.B.L.J., R.M.), Ohio University College of Arts and Sciences, Athens, Ohio 45701; Biomedical Engineer
Endocrinology ; 156(2): 453-61, 2015 Feb.
Article en En | MEDLINE | ID: mdl-25422874
Group B coxsackieviruses (CVBs) are involved in triggering some cases of type 1 diabetes mellitus (T1DM). However, the molecular mechanism(s) responsible for this remain elusive. Toll-like receptor 3 (TLR3), a receptor that recognizes viral double-stranded RNA, is hypothesized to play a role in virus-induced T1DM, although this hypothesis is yet to be substantiated. The objective of this study was to directly investigate the role of TLR3 in CVB-triggered T1DM in nonobese diabetic (NOD) mice, a mouse model of human T1DM that is widely used to study both spontaneous autoimmune and viral-induced T1DM. As such, we infected female wild-type (TLR3(+/+)) and TLR3 knockout (TLR3(-/-)) NOD mice with CVB4 and compared the incidence of diabetes in CVB4-infected mice with that of uninfected counterparts. We also evaluated the islets of uninfected and CVB4-infected wild-type and TLR3 knockout NOD mice by immunohistochemistry and insulitis scoring. TLR3 knockout mice were markedly protected from CVB4-induced diabetes compared with CVB4-infected wild-type mice. CVB4-induced T-lymphocyte-mediated insulitis was also significantly less severe in TLR3 knockout mice compared with wild-type mice. No differences in insulitis were observed between uninfected animals, either wild-type or TLR3 knockout mice. These data demonstrate for the first time that TLR3 is 1) critical for CVB4-induced T1DM, and 2) modulates CVB4-induced insulitis in genetically prone NOD mice.
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Infecciones por Coxsackievirus / Diabetes Mellitus Tipo 1 / Receptor Toll-Like 3 Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Endocrinology Año: 2015 Tipo del documento: Article Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Infecciones por Coxsackievirus / Diabetes Mellitus Tipo 1 / Receptor Toll-Like 3 Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Endocrinology Año: 2015 Tipo del documento: Article Pais de publicación: Estados Unidos