Allergy · 2026
MAIT Cells Suppress IgE-Mediated Asthma via IFNγ-Dependent B Cell Regulation.
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Cannata Angela M, McAlees Jaclyn W, Hargis Julie M, Shankar Archana, Huang Shouxiong, Divanovic Senad, Lewkowich Ian P
Аннотация
BACKGROUND: Mucosal-associated invariant T (MAIT) cells are innate-like lymphocytes enriched in mucosal tissues, but their role in allergic asthma pathogenesis remains poorly defined. In this study, we sought to elucidate the role of MAIT cells in a T cell-dominant model of allergic asthma.
METHODS: We used a murine model of house dust mite-induced asthma and a selective MAIT cell antagonist (Acetyl-6-formylpterin, A6FP) to inhibit MAIT cell activation in vivo. Airway hyperresponsiveness, lung inflammation, serum IgE, and cytokine profiles were assessed. In vitro co-culture experiments evaluated the direct impact of MAIT cells on B cell IgE production.
RESULTS: Pharmacologic inhibition of MAIT cells exacerbated airway hyperresponsiveness and elevated circulating IgE without altering airway eosinophilia or T helper type 2/type 17 cytokine production. MAIT cell antagonism failed to increase AHR in IgE-deficient mice. In vitro, activated MAIT cells directly suppressed B cell IgE production through IFNγ signaling. IL-4 was sufficient to enhance IFNγ production by MAIT cells, suggesting that allergic inflammation may induce a counter-regulatory response from MAIT cells to limit IgE-mediated pathology.
CONCLUSION: MAIT cells limit airway hyperresponsiveness by suppressing IgE production through IFNγ-dependent B cell regulation. These findings define a previously unrecognized immunoregulatory function of MAIT cells in allergic asthma and suggest that enhancing MAIT cell activity may represent a therapeutic strategy for IgE-mediated diseases.
METHODS: We used a murine model of house dust mite-induced asthma and a selective MAIT cell antagonist (Acetyl-6-formylpterin, A6FP) to inhibit MAIT cell activation in vivo. Airway hyperresponsiveness, lung inflammation, serum IgE, and cytokine profiles were assessed. In vitro co-culture experiments evaluated the direct impact of MAIT cells on B cell IgE production.
RESULTS: Pharmacologic inhibition of MAIT cells exacerbated airway hyperresponsiveness and elevated circulating IgE without altering airway eosinophilia or T helper type 2/type 17 cytokine production. MAIT cell antagonism failed to increase AHR in IgE-deficient mice. In vitro, activated MAIT cells directly suppressed B cell IgE production through IFNγ signaling. IL-4 was sufficient to enhance IFNγ production by MAIT cells, suggesting that allergic inflammation may induce a counter-regulatory response from MAIT cells to limit IgE-mediated pathology.
CONCLUSION: MAIT cells limit airway hyperresponsiveness by suppressing IgE production through IFNγ-dependent B cell regulation. These findings define a previously unrecognized immunoregulatory function of MAIT cells in allergic asthma and suggest that enhancing MAIT cell activity may represent a therapeutic strategy for IgE-mediated diseases.