PortalPublikationenMucosal-associated invariant T cells contribute to suppressi...

Mucosal-associated invariant T cells contribute to suppression of inflammatory myeloid cells in immune-mediated kidney disease

Standard

Mucosal-associated invariant T cells contribute to suppression of inflammatory myeloid cells in immune-mediated kidney disease. / Gnirck, Ann-Christin; Philipp, Marie-Sophie; Waterhölter, Alex; Wunderlich, Malte; Shaikh, Nikhat; Adamiak, Virginia; Henneken, Lena; Kautz, Tobias; Xiong, Tingting; Klaus, Daniela; Tomczyk, Pascal; Al-Bahra, Mohamad M; Menche, Dirk; Walkenhorst, Mark; Lantz, Olivier; Willing, Anne; Friese, Manuel A; Huber, Tobias B; Krebs, Christian F; Panzer, Ulf; Kurts, Christian; Turner, Jan-Eric.

in: NAT COMMUN, Jahrgang 14, Nr. 1, 7372, 15.11.2023.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Gnirck, A-C, Philipp, M-S, Waterhölter, A, Wunderlich, M, Shaikh, N, Adamiak, V, Henneken, L, Kautz, T, Xiong, T, Klaus, D, Tomczyk, P, Al-Bahra, MM, Menche, D, Walkenhorst, M, Lantz, O, Willing, A, Friese, MA, Huber, TB, Krebs, CF, Panzer, U, Kurts, C & Turner, J-E 2023, 'Mucosal-associated invariant T cells contribute to suppression of inflammatory myeloid cells in immune-mediated kidney disease', NAT COMMUN, Jg. 14, Nr. 1, 7372. https://doi.org/10.1038/s41467-023-43269-0

APA

Gnirck, A-C., Philipp, M-S., Waterhölter, A., Wunderlich, M., Shaikh, N., Adamiak, V., Henneken, L., Kautz, T., Xiong, T., Klaus, D., Tomczyk, P., Al-Bahra, M. M., Menche, D., Walkenhorst, M., Lantz, O., Willing, A., Friese, M. A., Huber, T. B., Krebs, C. F., ... Turner, J-E. (2023). Mucosal-associated invariant T cells contribute to suppression of inflammatory myeloid cells in immune-mediated kidney disease. NAT COMMUN, 14(1), [7372]. https://doi.org/10.1038/s41467-023-43269-0

Vancouver

Gnirck A-C, Philipp M-S, Waterhölter A, Wunderlich M, Shaikh N, Adamiak V et al. Mucosal-associated invariant T cells contribute to suppression of inflammatory myeloid cells in immune-mediated kidney disease. NAT COMMUN. 2023 Nov 15;14(1). 7372. https://doi.org/10.1038/s41467-023-43269-0

Bibtex

@article{88c3c0fadbf343b88900af85dcbf24a0,
title = "Mucosal-associated invariant T cells contribute to suppression of inflammatory myeloid cells in immune-mediated kidney disease",
abstract = "Mucosal-associated invariant T (MAIT) cells have been implicated in various inflammatory diseases of barrier organs, but so far, their role in kidney disease is unclear. Here we report that MAIT cells that recognize their prototypical ligand, the vitamin B2 intermediate 5-OP-RU presented by MR1, reside in human and mouse kidneys. Single cell RNAseq analysis reveals several intrarenal MAIT subsets, and one, carrying the genetic fingerprint of tissue-resident MAIT17 cells, is activated and expanded in a murine model of crescentic glomerulonephritis (cGN). An equivalent subset is also present in kidney biopsies of patients with anti-neutrophil cytoplasmatic antibody (ANCA)-associated cGN. MAIT cell-deficient MR1 mice show aggravated disease, whereas B6-MAITCAST mice, harboring higher MAIT cell numbers, are protected from cGN. The expanded MAIT17 cells express anti-inflammatory mediators known to suppress cGN, such as CTLA-4, PD-1, and TGF-β. Interactome analysis predicts CXCR6 - CXCL16-mediated cross-talk with renal mononuclear phagocytes, known to drive cGN progression. In line, we find that cGN is aggravated upon CXCL16 blockade. Finally, we present an optimized 5-OP-RU synthesis method which we apply to attenuating cGN in mice. In summary, we propose that CXCR6+ MAIT cells might play a protective role in cGN, implicating them as a potential target for anti-inflammatory therapies.",
keywords = "Humans, Animals, Mice, Mucosal-Associated Invariant T Cells, Myeloid Cells/metabolism, Kidney Diseases/metabolism, Anti-Inflammatory Agents/metabolism, Histocompatibility Antigens Class I/metabolism",
author = "Ann-Christin Gnirck and Marie-Sophie Philipp and Alex Waterh{\"o}lter and Malte Wunderlich and Nikhat Shaikh and Virginia Adamiak and Lena Henneken and Tobias Kautz and Tingting Xiong and Daniela Klaus and Pascal Tomczyk and Al-Bahra, {Mohamad M} and Dirk Menche and Mark Walkenhorst and Olivier Lantz and Anne Willing and Friese, {Manuel A} and Huber, {Tobias B} and Krebs, {Christian F} and Ulf Panzer and Christian Kurts and Jan-Eric Turner",
note = "{\textcopyright} 2023. The Author(s).",
year = "2023",
month = nov,
day = "15",
doi = "10.1038/s41467-023-43269-0",
language = "English",
volume = "14",
journal = "NAT COMMUN",
issn = "2041-1723",
publisher = "NATURE PUBLISHING GROUP",
number = "1",

}

RIS

TY - JOUR

T1 - Mucosal-associated invariant T cells contribute to suppression of inflammatory myeloid cells in immune-mediated kidney disease

AU - Gnirck, Ann-Christin

AU - Philipp, Marie-Sophie

AU - Waterhölter, Alex

AU - Wunderlich, Malte

AU - Shaikh, Nikhat

AU - Adamiak, Virginia

AU - Henneken, Lena

AU - Kautz, Tobias

AU - Xiong, Tingting

AU - Klaus, Daniela

AU - Tomczyk, Pascal

AU - Al-Bahra, Mohamad M

AU - Menche, Dirk

AU - Walkenhorst, Mark

AU - Lantz, Olivier

AU - Willing, Anne

AU - Friese, Manuel A

AU - Huber, Tobias B

AU - Krebs, Christian F

AU - Panzer, Ulf

AU - Kurts, Christian

AU - Turner, Jan-Eric

N1 - © 2023. The Author(s).

PY - 2023/11/15

Y1 - 2023/11/15

N2 - Mucosal-associated invariant T (MAIT) cells have been implicated in various inflammatory diseases of barrier organs, but so far, their role in kidney disease is unclear. Here we report that MAIT cells that recognize their prototypical ligand, the vitamin B2 intermediate 5-OP-RU presented by MR1, reside in human and mouse kidneys. Single cell RNAseq analysis reveals several intrarenal MAIT subsets, and one, carrying the genetic fingerprint of tissue-resident MAIT17 cells, is activated and expanded in a murine model of crescentic glomerulonephritis (cGN). An equivalent subset is also present in kidney biopsies of patients with anti-neutrophil cytoplasmatic antibody (ANCA)-associated cGN. MAIT cell-deficient MR1 mice show aggravated disease, whereas B6-MAITCAST mice, harboring higher MAIT cell numbers, are protected from cGN. The expanded MAIT17 cells express anti-inflammatory mediators known to suppress cGN, such as CTLA-4, PD-1, and TGF-β. Interactome analysis predicts CXCR6 - CXCL16-mediated cross-talk with renal mononuclear phagocytes, known to drive cGN progression. In line, we find that cGN is aggravated upon CXCL16 blockade. Finally, we present an optimized 5-OP-RU synthesis method which we apply to attenuating cGN in mice. In summary, we propose that CXCR6+ MAIT cells might play a protective role in cGN, implicating them as a potential target for anti-inflammatory therapies.

AB - Mucosal-associated invariant T (MAIT) cells have been implicated in various inflammatory diseases of barrier organs, but so far, their role in kidney disease is unclear. Here we report that MAIT cells that recognize their prototypical ligand, the vitamin B2 intermediate 5-OP-RU presented by MR1, reside in human and mouse kidneys. Single cell RNAseq analysis reveals several intrarenal MAIT subsets, and one, carrying the genetic fingerprint of tissue-resident MAIT17 cells, is activated and expanded in a murine model of crescentic glomerulonephritis (cGN). An equivalent subset is also present in kidney biopsies of patients with anti-neutrophil cytoplasmatic antibody (ANCA)-associated cGN. MAIT cell-deficient MR1 mice show aggravated disease, whereas B6-MAITCAST mice, harboring higher MAIT cell numbers, are protected from cGN. The expanded MAIT17 cells express anti-inflammatory mediators known to suppress cGN, such as CTLA-4, PD-1, and TGF-β. Interactome analysis predicts CXCR6 - CXCL16-mediated cross-talk with renal mononuclear phagocytes, known to drive cGN progression. In line, we find that cGN is aggravated upon CXCL16 blockade. Finally, we present an optimized 5-OP-RU synthesis method which we apply to attenuating cGN in mice. In summary, we propose that CXCR6+ MAIT cells might play a protective role in cGN, implicating them as a potential target for anti-inflammatory therapies.

KW - Humans

KW - Animals

KW - Mice

KW - Mucosal-Associated Invariant T Cells

KW - Myeloid Cells/metabolism

KW - Kidney Diseases/metabolism

KW - Anti-Inflammatory Agents/metabolism

KW - Histocompatibility Antigens Class I/metabolism

U2 - 10.1038/s41467-023-43269-0

DO - 10.1038/s41467-023-43269-0

M3 - SCORING: Journal article

C2 - 37968302

VL - 14

JO - NAT COMMUN

JF - NAT COMMUN

SN - 2041-1723

IS - 1

M1 - 7372

ER -