MAIT cells in metabolic diseases. Mol Metab. 2019 Sep;27S:S114-S121 Authors: Bertrand L, Lehuen A Abstract PMID: 31500822 [PubMed - in process] Mucosal-associated invariant T cells and disease. Nat Rev Immunol. 2019 Jul 15;: Authors: Toubal A, Nel I, Lotersztajn S, Lehuen A Abstract PMID: 31308521 [PubMed - as supplied by publisher]
BACKGROUND: Metabolic diseases represent a wide category of alterations affecting metabolism. These pathologies are notably marked by inflammation that implicates the immune system. Mucosal Associated Invariant (MAI)T cells are immune cells expressing a semi-invariant TCR able to recognize bacterial and fungal vitamin B metabolites. MAIT cells can promote inflammation and are present in many organs central to metabolism, suggesting a role in the etiopathology of these diseases.
SCOPE OF THE REVIEW: Here, we will review what is known of the involvement of MAIT cells in metabolic pathologies in humans and mice.
MAJOR CONCLUSIONS: MAIT cells are severely affected, overactivated with a frequency reduction and a phenotype shift from protective to deleterious. Therefore, they might be a novel target to treat, in particular, pancreas and liver metabolic diseases.
Mucosal-associated invariant T (MAIT) cells are unique innate-like T cells that bridge innate and adaptive immunity. They are activated by conserved bacterial ligands derived from vitamin B biosynthesis and have important roles in defence against bacterial and viral infections. However, they can also have various deleterious and protective functions in autoimmune, inflammatory and metabolic diseases. MAIT cell involvement in a large spectrum of pathological conditions makes them attractive targets for potential therapeutic approaches.
MAIT cells in metabolic diseases.
Mol Metab. 2019 Sep;27S:S114-S121
Authors: Bertrand L, Lehuen A
PMID: 31500822 [PubMed - in process]
Mucosal-associated invariant T cells and disease.
Nat Rev Immunol. 2019 Jul 15;:
Authors: Toubal A, Nel I, Lotersztajn S, Lehuen A
PMID: 31308521 [PubMed - as supplied by publisher]
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