New-onset type 1 diabetes and severe acute respiratory syndrome coronavirus 2 infection

Roy, Anindya (2023) New-onset type 1 diabetes and severe acute respiratory syndrome coronavirus 2 infection. Immunology & Cell Biology, 101 (3). pp. 191-203. ISSN 0818-9641

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Abstract

Type 1 diabetes (T1D) is a condition characterized by an absolute deficiency of insulin. Loss of insulin-producing pancreatic islet β cells is one of the many causes of T1D. Viral infections have long been associated with new-onset T1D and the balance between virulence and host immunity determines whether the viral infection would lead to T1D. Herein, we detail the dynamic interaction of pancreatic β cells with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the host immune system with respect to new-onset T1D. Importantly, β cells express the crucial entry receptors and multiple studies confirmed that β cells are infected by SARS-CoV-2. Innate immune system effectors, such as natural killer cells, can eliminate such infected β cells. Although CD4+CD25+FoxP3+ regulatory T (TREG) cells provide immune tolerance to prevent the destruction of the islet β-cell population by autoantigen-specific CD8+ T cells, it can be speculated that SARS-CoV-2 infection may compromise self-tolerance by depleting TREG-cell numbers or diminishing TREG-cell functions by repressing Forkhead box P3 (FoxP3) expression. However, the expansion of β cells by self-duplication, and regeneration from progenitor cells, could effectively replace lost β cells. Appearance of islet autoantibodies following SARS-CoV-2 infection was reported in a few cases, which could imply a breakdown of immune tolerance in the pancreatic islets. However, many of the cases with newly diagnosed autoimmune response following SARS-CoV-2 infection also presented with significantly high HbA1c (glycated hemoglobin) levels that indicated progression of an already set diabetes, rather than new-onset T1D. Here we review the potential underlying mechanisms behind loss of functional β-cell mass as a result of SARS-CoV-2 infection that can trigger new-onset T1D.

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IITH Creators:

IITH Creators	ORCiD
Roy, Anindya	http://orcid.org/0000-0001-8561-907X

Item Type:

Article

Uncontrolled Keywords:

autoimmune response; COVID-19; new-onset diabetes; pancreatic islet β cells; SARS-CoV-2; type 1 diabetes; CD8-Positive T-Lymphocytes; COVID-19; Diabetes Mellitus, Type 1; Forkhead Transcription Factors; Humans; Insulin; SARS-CoV-2; T-Lymphocytes, Regulatory; Virus Diseases; interferon; forkhead transcription factor; insulin; cell damage; cell specificity; coronavirus disease 2019; dendritic cell; human; immune response; immunological tolerance; insulin dependent diabetes mellitus; new onset type 1 diabetes; nonhuman; pancreas islet beta cell; Review; CD8+ T lymphocyte; insulin dependent diabetes mellitus; metabolism; regulatory T lymphocyte; virus infection

Subjects:

Others > Biotechnology

Divisions:

Department of Biotechnology

Depositing User:

Mr Nigam Prasad Bisoyi

Date Deposited:

24 Aug 2023 10:38

Last Modified:

24 Aug 2023 10:38

URI:

http://raiithold.iith.ac.in/id/eprint/11614