Islet inflammation and CXCL10 in recent-onset type 1 diabetes
Rattachement africain : nl, it. Niveau de preuve : code pays fourni par la source.
Le résumé fourni par la source
Type 1 diabetes results from a T cell-mediated destruction of insulin-producing pancreatic beta cells. Little is known on local factors contributing to migration of T cells to pancreatic tissue. We recently demonstrated evidence of viral infection in beta cells in several recent-onset type 1 diabetes patients. Islet inflammation was analysed in a series of new- or recent-onset type 1 diabetic patients and non-diabetic control subjects. Autoimmune T cell reactivity was studied in lymphocytes derived from pancreas-draining lymph nodes of one recent-onset type 1 diabetes patient in partial clinical remission. Insulitic lesions were characterized by presence of beta cells, elevated levels of the chemokine CXCL10 and infiltration of lymphocytes expressing the corresponding chemokine receptor CXCR3 in all pancreatic lesions of type 1 diabetes patients, regardless of enterovirus infection of beta cells. CXCR3 and CXCL10 were undetectable in pancreata of non-diabetic control subjects. T cells isolated from draining lymph nodes of a recent-onset patient with virally infected beta cells and in clinical remission reacted with multiple islet autoantigens and displayed a mixed interferon (IFN)-gamma/interleukin (IL)-10 cytokine pattern. Our data point to CXCL10 as an important cytokine in distressed islets that may contribute to inflammation leading to insulitis and beta cell destruction, regardless of local viral infection. We demonstrate further pro- and anti-inflammatory islet autoreactivity, indicating that different adaptive and innate immune responses may contribute to insulitis and beta cell destruction.
Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.
Le contrôle bibliographique ouvert
DOI retrouvé dans Crossref DOI retrouvé ; titre concordant.
- Titre Crossref
- Islet inflammation and CXCL10 in recent-onset type 1 diabetes
- Date Crossref
- 05/01/2010
- Éditeur
- Oxford University Press (OUP)
- Type
- journal-article
Ce recoupement confirme des métadonnées liées au DOI. Il ne confirme ni la méthode ni les conclusions de l’étude, et il ne compte pas comme une seconde source scientifique indépendante.
Où se fait cette recherche
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Leiden University Medical Center Department of Immunohaematology and Blood Transfusion pays non établi dans la noticeOrganisme public
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University of Siena Department of Internal Medicine and of Endocrine and Metabolic Sciences pays non établi dans la noticeUniversité ou école supérieure
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Fondazione Umberto Di Mario pays non établi dans la noticeStructure de recherche
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University of Pisa Department of Endocrinology and Metabolism-Metabolic Unit pays non établi dans la noticeUniversité ou école supérieure
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Ospedale Cisanello pays non établi dans la noticeÉtablissement de santé
Department of Immunohaematology and Blood Transfusion — Leiden University Medical Center, Department of Internal Medicine and of Endocrine and Metabolic Sciences — University of Siena et Fondazione Umberto Di Mario, avec 2 autres affiliations.
Une affiliation ne permet pas de déduire la nationalité d’un auteur.