Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2025 May 30:16:1594712.
doi: 10.3389/fimmu.2025.1594712. eCollection 2025.

Control of MAIT cell functions by cytokines in health and disease

Laetitia Camard  1 , Elisabetta Bianchi  1 , Lars Rogge  1
Affiliations
Review

Control of MAIT cell functions by cytokines in health and disease

Laetitia Camard et al. Front Immunol. .

Abstract

Mucosal-associated invariant T (MAIT) cells are innate-like T cells that express a semi-invariant T cell receptor (TCR). These cells predominantly reside in tissues, such as the liver, lung, skin and the gastrointestinal tract. MAIT cells can be activated via their TCR that recognizes riboflavin metabolites presented by the MHC class I-related protein 1 (MR1). These cells can also be activated in a TCR-independent manner by cytokines, in particular IL-12 and IL-18, but also by type I interferons, IL-7, IL-15 and IL-23, underlining their innate-like characteristics. MAIT cells have important functions in antibacterial and viral immunity but also in tissue repair and homeostasis. Recent studies highlighted the plasticity of MAIT cells in response to cytokines, suggesting an important role of the cytokine milieu in modulating MAIT cell functions. Here, we discuss how cytokines control MAIT cell functions in various contexts.

Keywords: Cytokines; MAIT cell activation; MAIT cells; cell plasticity; infectious diseases; inflammatory diseases; interleukins; tissue repair.

PubMed Disclaimer

Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Control of MAIT cell functions by cytokines. Summary of the effects of cytokines on MAIT cell functions. MAIT cells can be activated in the absence of a TCR stimulus (left panel) by cytokines such as IL-7, IL-18, IL-15, type I interferons or the combination of IL-12+IL-18. MAIT cells exhibit various responses to cytokines as they can secrete pro-inflammatory cytokines (e.g. IFN-γ), cytotoxic mediators or adopt a tissue repair program. The cytokine milieu can also influence MAIT cell functions in the presence of a TCR stimulus (right panel). MAIT cells can adopt distinct functional and transcriptional profiles in response to different cytokines, highlighting their plasticity.
See this image and copyright information in PMC

References

    1. Tilloy F, Treiner E, Park S-H, Garcia C, Lemonnier F, de la Salle H, et al. An invariant T cell receptor α Chain defines a novel TAP-independent major histocompatibility complex class Ib–restricted α/β T cell subpopulation in mammals. J Exp Med. (1999) 189:1907–21. doi: 10.1084/jem.189.12.1907 - DOI - PMC - PubMed
    1. Treiner E, Duban L, Bahram S, Radosavljevic M, Wanner V, Tilloy F, et al. Selection of evolutionarily conserved mucosal-associated invariant T cells by MR1. Nature. (2003) 422:164–9. doi: 10.1038/nature01433 - DOI - PubMed
    1. Kjer-Nielsen L, Patel O, Corbett AJ, Le Nours J, Meehan B, Liu L, et al. MR1 presents microbial vitamin B metabolites to MAIT cells. Nature. (2012) 491:717–23. doi: 10.1038/nature11605 - DOI - PubMed
    1. Corbett AJ, Eckle SBG, Birkinshaw RW, Liu L, Patel O, Mahony J, et al. T-cell activation by transitory neo-antigens derived from distinct microbial pathways. Nature. (2014) 509:361–5. doi: 10.1038/nature13160 - DOI - PubMed
    1. Boudinot P, Mondot S, Jouneau L, Teyton L, Lefranc M-P, Lantz O. Restricting nonclassical MHC genes coevolve with TRAV genes used by innate-like T cells in mammals. Proc Natl Acad Sci. (2016) 113:E2983–92. doi: 10.1073/pnas.1600674113 - DOI - PMC - PubMed

MeSH terms

LinkOut - more resources