Abstract
Hypomorphic Rag mutations in humans cause Omenn Syndrome (OS) a severe immunodeficiency associated with autoimmune-like manifestations mediated by oligoclonal activated T and B cells. The clinical and immunological spectrum of OS presentation is extremely broad. However, the role played by environmental triggers in the disease pathogenesis remains largely unknown. We have recently shown in a murine model that gut microbiota has a substantial role in determining the distinctive immune dysregulation of OS. Here, we describe how dysbiosis and loss of T cell tolerance to commensals influence the expression of autoimmunity at the barrier site and beyond, and the disease hallmark hyper-IgE. We discuss how commensal antigens and gut-derived pathogenic T cells could potentially modulate skin immunity to determine cutaneous degenerations in OS. These mechanisms may have broader implications for a deeper understanding of the role of gut microbes in influencing barriers integrity and host physiology.
Original language | English |
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Pages (from-to) | 1-9 |
Number of pages | 9 |
Journal | Gut Microbes |
DOIs | |
Publication status | Accepted/In press - Sept 11 2016 |
Keywords
- commensal bacteria
- dysbiosis
- hyperIgE
- IgA deficiency
- immunodeficiency
- RAG
- T and B cell autoimmunity
ASJC Scopus subject areas
- Gastroenterology
- Infectious Diseases
- Microbiology (medical)
- Microbiology