title: Mucosal-Associated Invariant T (MAIT) Cells Are Impaired in Th17 Associated Primary and Secondary Immunodeficiencies.
abstract: The recently described Mucosal Associated Invariant T (MAIT) cells mediate specific recognition of bacterial and fungal vitamin B2 metabolites. As innate T cells, they possess broad effector responses, including IFN- including Iproduction, that are comparable to conventional T cell responses. Immunodeficiencies associated with systemic Th17 deficiency may also be compounded by defects in MAIT immunity. We evaluated Th17 immunity in this innate T cell compartment in primary (AD-HIES) and secondary immunodeficiency (thymoma) patients with conventional Th17 deficiency and susceptibility to fungal and bacterial disease. Our results suggest that MAIT cells are both reduced and functional deficient in STAT3 deficiency and thymoma patients with IL-12/23 autoantibodies. In contrast, thymoma patients without autoantibodies preserved the normal number and functional MAIT cells.
authors.affiliation: Academic Unit of Cancer Sciences, Faculty of Medicine, University of Southampton and Southampton NIHR Experimental Cancer Medicine Centre, Southampton, United Kingdom.
authors.forename: Yifang
authors.initials: Y
authors.lastname: Gao
authors.affiliation: Department of Clinical Immunology, University Hospital Southampton NHS Foundation Trust, Southampton, United Kingdom.
authors.forename: William
authors.initials: W
authors.lastname: Rae
authors.affiliation: Academic Unit of Cancer Sciences, Faculty of Medicine, University of Southampton and Southampton NIHR Experimental Cancer Medicine Centre, Southampton, United Kingdom.
authors.forename: Keseva Ananth
authors.initials: KA
authors.lastname: Ramakrishnan
authors.affiliation: Department of Clinical Immunology, Addenbrookes Hospital, Cambridge, United Kingdom.
authors.forename: Gabriela
authors.initials: G
authors.lastname: Barcenas-Morales
authors.affiliation: Department of Clinical Immunology, Addenbrookes Hospital, Cambridge, United Kingdom.
authors.forename: Rainer
authors.initials: R
authors.lastname: Döffinger
authors.affiliation: Department of Clinical Immunology, University Hospital Southampton NHS Foundation Trust, Southampton, United Kingdom.
authors.forename: Efrem
authors.initials: E
authors.lastname: Eren
authors.affiliation: NIHR Wellcome Trust Clinical Research Facility, University Hospital Southampton NHS Foundation Trust, Southampton, United Kingdom.
authors.forename: Saul N
authors.initials: SN
authors.lastname: Faust
authors.affiliation: Academic Unit of Cancer Sciences, Faculty of Medicine, University of Southampton and Southampton NIHR Experimental Cancer Medicine Centre, Southampton, United Kingdom.
authors.forename: Christian H
authors.initials: CH
authors.lastname: Ottensmeier
authors.affiliation: Academic Unit of Cancer Sciences, Faculty of Medicine, University of Southampton and Southampton NIHR Experimental Cancer Medicine Centre, Southampton, United Kingdom.|Department of Clinical Immunology, University Hospital Southampton NHS Foundation Trust, Southampton, United Kingdom.
authors.forename: Anthony P
authors.initials: AP
authors.lastname: Williams
mesh_terms: D000328:Adult; D000368:Aged; D016022:Case-Control Studies; D016207:Cytokines / Q000096:biosynthesis; D005260:Female; D006801:Humans; D007153:Immunologic Deficiency Syndromes / Q000276:immunology*; D042541:Intracellular Space / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D000072336:Mucosal-Associated Invariant T Cells / Q000276:immunology*; D058504:Th17 Cells / Q000276:immunology*
chemical_list: D016207:Cytokines