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© Charles DAUGUET, Institut Pasteur
HIV particles
Publication : Science advances

Sustained IFN-I stimulation impairs MAIT cell responses to bacteria by inducing IL-10 during chronic HIV-1 infection.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Science advances - 01 Feb 2020

Tang X, Zhang S, Peng Q, Ling L, Shi H, Liu Y, Cheng L, Xu L, Cheng L, Chakrabarti LA, Chen Z, Wang H, Zhang Z,

Link to Pubmed [PMID] – 32128419

Link to DOI – 10.1126/sciadv.aaz0374

Sci Adv 2020 02; 6(8): eaaz0374

Mucosal-associated invariant T (MAIT) cells in HIV-1-infected individuals are functionally impaired by poorly understood mechanisms. Single-cell transcriptional and surface protein analyses revealed that peripheral MAIT cells from HIV-1-infected subjects were highly activated with the up-regulation of interferon (IFN)-stimulated genes as compared to healthy individuals. Sustained IFN-α treatment suppressed MAIT cell responses to Escherichia coli by triggering high-level interleukin-10 (IL-10) production by monocytes, which subsequently inhibited the secretion of IL-12, a crucial costimulatory cytokine for MAIT cell activation. Blocking IFN-α or IL-10 receptors prevented MAIT cell dysfunction induced by HIV-1 exposure in vitro. Moreover, blocking the IL-10 receptor significantly improved anti-Mycobacterium tuberculosis responses of MAIT cells from HIV-1-infected patients. Our findings demonstrate the central role of the IFN-I/IL-10 axis in MAIT cell dysfunction during HIV-1 infection, which has implications for the development of anti-IFN-I/IL-10 strategies against bacterial coinfections in HIV-1-infected patients.

https://pubmed.ncbi.nlm.nih.gov/32128419