Group B coxsackieviruses and autoimmunity: focus on Type 1 diabetes

Abstract

Group B coxsackieviruses (CVB) and/or their components have been found in the blood and pancreas of patients with Type 1 diabetes (T1D). CVB infections lead to the activation of the innate and adaptive immune systems, which can result in the induction or aggravation of autoimmune processes. Persistent and/or repeated infections of pancreas islet β cells with CVB and the resulting production of IFN-α and inflammatory mediators, combined with a predisposed genetic background, may induce bystander activation of autoimmune effector T cells and an autoreactive response to islet self-antigens through molecular mimicry. Moreover, the antibody-dependent enhancement of CVB infection of monocytes, as well as infection of the thymus can intervene in the pathogenesis of T1D. In contrast with the deleterious effect of CVB, it has been shown that these viruses can protect against the development of T1D under certain experimental conditions. The role of CVB in autoimmunity is complex, and therefore a better understanding of the inducer versus protective effects of these viruses in T1D will help to design new strategies to treat and prevent the disease.

Keywords::

• autoimmunity
• Group B coxsackieviruses
• islet β cells
• Type 1 diabetes

Acknowledgements

The authors thank Delphine Caloone for technical assistance and all their other collaborators.

Ilham Moumna’s present address is Centre d’Investigation Clinique, Hôpital Cardiologique, CHRU de Lille, France.

Financial & competing interests disclosure

The studies performed by the authors were supported by EU FP6 Integrated Project EURO-THYMAIDE (Contract LSHB-CT-2003-503410), EU FP5 VIRDIAB Project (Contract QLK 2-CT-2001-01910), a grant from Nord-Pas-de-Calais Région (ArCir convention 2004/018), CHRU Lille, the ministère de l’Education Nationale de la Recherche et de la Technologie, Université de Lille-II, France, and the Comité Mixte de Coopération Universitaire Franco-Tunisien (CMCU 2004 No 04/G0810 and CMCU 2008N808/G0808). Didier Hober was the ALFEDIAM/Novartis 2002 and ALFEDIAM/Roche 2003 prize winner and Fondation pour la Recherche Médicale 2008 prize winner. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

No writing assistance was utilized in the production of this manuscript.