Differential cell autonomous responses determine the outcome of coxsackievirus infections in murine pancreatic α and β cells

Author:

Marroqui Laura1,Lopes Miguel1,dos Santos Reinaldo S1,Grieco Fabio A1,Roivainen Merja2,Richardson Sarah J3,Morgan Noel G3,Op de beeck Anne1,Eizirik Decio L1

Affiliation:

1. ULB Center for Diabetes Research, Medical Faculty, Université Libre de Bruxelles, Brussels, Belgium

2. National Institute for Health and Welfare, Helsinki, Finland

3. Institute of Biomedical and Clinical Sciences, University of Exeter Medical School, Exeter, United Kingdom

Abstract

Type 1 diabetes (T1D) is an autoimmune disease caused by loss of pancreatic β cells via apoptosis while neighboring α cells are preserved. Viral infections by coxsackieviruses (CVB) may contribute to trigger autoimmunity in T1D. Cellular permissiveness to viral infection is modulated by innate antiviral responses, which vary among different cell types. We presently describe that global gene expression is similar in cytokine-treated and virus-infected human islet cells, with up-regulation of gene networks involved in cell autonomous immune responses. Comparison between the responses of rat pancreatic α and β cells to infection by CVB5 and 4 indicate that α cells trigger a more efficient antiviral response than β cells, including higher basal and induced expression of STAT1-regulated genes, and are thus better able to clear viral infections than β cells. These differences may explain why pancreatic β cells, but not α cells, are targeted by an autoimmune response during T1D.

Funder

Fonds De La Recherche Scientifique - FNRS

European Commission (EC)

Fédération Wallonie-Bruxelles

Governo Brasil

Juvenile Diabetes Research Foundation International (JDRF)

Publisher

eLife Sciences Publications, Ltd

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine,General Neuroscience

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