New-onset type 1 diabetes and severe acute respiratory syndrome coronavirus 2 infection.
Immunol Cell Biol
; 101(3): 191-203, 2023 03.
Artículo
en Inglés
| MEDLINE | ID: covidwho-2249670
ABSTRACT
Type 1 diabetes (T1D) is a condition characterized by an absolute deficiency of insulin. Loss of insulin-producing pancreatic islet ß 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 ß cells with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and the host immune system with respect to new-onset T1D. Importantly, ß cells express the crucial entry receptors and multiple studies confirmed that ß cells are infected by SARS-CoV-2. Innate immune system effectors, such as natural killer cells, can eliminate such infected ß cells. Although CD4+ CD25+ FoxP3+ regulatory T (TREG ) cells provide immune tolerance to prevent the destruction of the islet ß-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 ß cells by self-duplication, and regeneration from progenitor cells, could effectively replace lost ß 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 ß-cell mass as a result of SARS-CoV-2 infection that can trigger new-onset T1D.
Palabras clave
Texto completo:
Disponible
Colección:
Bases de datos internacionales
Base de datos:
MEDLINE
Asunto principal:
Virosis
/
Diabetes Mellitus Tipo 1
/
COVID-19
Límite:
Humanos
Idioma:
Inglés
Revista:
Immunol Cell Biol
Asunto de la revista:
Alergia e Inmunología
Año:
2023
Tipo del documento:
Artículo
País de afiliación:
Imcb.12615
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