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Mucosal-Associated Invariant T (MAIT) cells are impaired in Th17 associated primary and secondary immunodeficiencies

Mucosal-Associated Invariant T (MAIT) cells are impaired in Th17 associated primary and secondary immunodeficiencies
Mucosal-Associated Invariant T (MAIT) cells are impaired in Th17 associated primary and secondary immunodeficiencies
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.
1932-6203
1-9
Gao, Yifang
eea234ba-f566-4f21-a65e-234b84cba285
Rae, William
8746e0ae-b868-4356-9c89-fe78600cf427
Ramakrishnan, Keseva
70b9d064-65df-40b9-badf-c86d308f2313
Barcenas-Morales, Gabriela
eedd9c75-776a-4fe0-a06e-88621e56cb15
Döffinger, Rainer
0c37187c-0cea-4466-8dee-826315d19f14
Eren, Efrem
ac449fc8-4ae2-4efd-ad91-9dcea3f355e2
Faust, Saul N.
f97df780-9f9b-418e-b349-7adf63e150c1
Ottensmeier, Christian H.
42b8a398-baac-4843-a3d6-056225675797
Williams, Anthony P.
973ff46f-46f1-4d7c-b27d-0f53221e4c44
Gao, Yifang
eea234ba-f566-4f21-a65e-234b84cba285
Rae, William
8746e0ae-b868-4356-9c89-fe78600cf427
Ramakrishnan, Keseva
70b9d064-65df-40b9-badf-c86d308f2313
Barcenas-Morales, Gabriela
eedd9c75-776a-4fe0-a06e-88621e56cb15
Döffinger, Rainer
0c37187c-0cea-4466-8dee-826315d19f14
Eren, Efrem
ac449fc8-4ae2-4efd-ad91-9dcea3f355e2
Faust, Saul N.
f97df780-9f9b-418e-b349-7adf63e150c1
Ottensmeier, Christian H.
42b8a398-baac-4843-a3d6-056225675797
Williams, Anthony P.
973ff46f-46f1-4d7c-b27d-0f53221e4c44

Gao, Yifang, Rae, William, Ramakrishnan, Keseva, Barcenas-Morales, Gabriela, Döffinger, Rainer, Eren, Efrem, Faust, Saul N., Ottensmeier, Christian H. and Williams, Anthony P. (2016) Mucosal-Associated Invariant T (MAIT) cells are impaired in Th17 associated primary and secondary immunodeficiencies. PLoS ONE, 11 (5), 1-9. (doi:10.1371/journal.pone.0155059). (PMID:27167980)

Record type: Article

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.

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Accepted/In Press date: 23 April 2016
e-pub ahead of print date: 11 May 2016
Organisations: Cancer Sciences

Identifiers

Local EPrints ID: 396160
URI: http://eprints.soton.ac.uk/id/eprint/396160
ISSN: 1932-6203
PURE UUID: d8cf0b6e-ae34-4477-a874-d1aa75a53f84
ORCID for Saul N. Faust: ORCID iD orcid.org/0000-0003-3410-7642

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Date deposited: 07 Jun 2016 09:15
Last modified: 15 Mar 2024 03:26

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Contributors

Author: Yifang Gao
Author: William Rae
Author: Keseva Ramakrishnan
Author: Gabriela Barcenas-Morales
Author: Rainer Döffinger
Author: Efrem Eren
Author: Saul N. Faust ORCID iD

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