HERV-W and Mycobacterium avium subspecies paratuberculosis Are at Play in Pediatric Patients at Onset of Type 1 Diabetes
| Autor: | Mario Palermo, Pietro Manca, Leonardo Antonio Sechi, Davide Cossu, Marta Noli, Gianfranco Meloni |
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| Rok vydání: | 2021 |
| Předmět: |
Microbiology (medical)
proinsulin children T1D onset endocrine system diseases viruses Mycobacterium paratuberculosis Disease Biology medicine.disease_cause Article Autoimmunity Retrovirus medicine antibodies Immunology and Allergy molecular mimicry Epigenetics Molecular Biology General Immunology and Microbiology nutritional and metabolic diseases biology.organism_classification Mycobacterium avium subspecies paratuberculosis Molecular mimicry Infectious Diseases HERV-W Immunology peptides Etiology biology.protein Medicine Antibody |
| Zdroj: | Pathogens Volume 10 Issue 9 Pathogens, Vol 10, Iss 1135, p 1135 (2021) |
| ISSN: | 2076-0817 |
| Popis: | The etiology of T1D remains unknown, although a variety of etiological agents have been proposed as potential candidates to trigger autoimmunity in susceptible individuals. Emerging evidence has indicated that endogenous human retrovirus (HERV) may play a role in the disease etiopathogenesis although several epigenetic mechanisms keep most HERVs silenced, environmental stimuli such as infections may contribute to the transcriptional reactivation of HERV-Wand thus promote pathological conditions. Previous studies have indicated that also Mycobacterium avium subspecies paratuberculosis (MAP) could be a potential risk factor for T1D, particularly in the Sardinian population. In the present study, the humoral response against HERV-W envelope and MAP-derived peptides was analyzed to investigate their potential role in T1D etiopathogenesis, in a Sardinian population at T1D onset (n = 26), T1D (45) and an age-matched healthy population (n = 45). For the first time, a high serum-prevalence of anti-Map and anti-HERV-W Abs was observed in pediatric patients at onset of T1D compared to T1D patients and healthy controls. Our results support the hypothesis that external infections and internal reactivations are involved in the etiology of T1D, and that HERV-W activation may be induced by infectious agents such as MAP. |
| Databáze: | OpenAIRE |
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