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Human type 1 innate lymphoid cells accumulate in inflamed mucosal tissues. / Bernink, Jochem H.; Peters, Charlotte P.; Munneke, Marius et al.

In: Nature immunology, Vol. 14, No. 3, 2013, p. 221-229.

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@article{ead81feaaed14b8f8cc8685f017f67ac,
title = "Human type 1 innate lymphoid cells accumulate in inflamed mucosal tissues",
abstract = "Innate lymphoid cells (ILCs) are effectors of innate immunity and regulators of tissue modeling. Recently identified ILC populations have a cytokine expression pattern that resembles that of the helper T cell subsets T(H)2, T(H)17 and T(H)22. Here we describe a distinct ILC subset similar to T(H)1 cells, which we call 'ILC1'. ILC1 cells expressed the transcription factor T-bet and responded to interleukin 12 (IL-12) by producing interferon-γ (IFN-γ). ILC1 cells were distinct from natural killer (NK) cells as they lacked perforin, granzyme B and the NK cell markers CD56, CD16 and CD94, and could develop from RORγt(+) ILC3 under the influence of IL-12. The frequency of the ILC1 subset was much higher in inflamed intestine of people with Crohn's disease, which indicated a role for these IFN-γ-producing ILC1 cells in the pathogenesis of gut mucosal inflammation",
author = "Bernink, {Jochem H.} and Peters, {Charlotte P.} and Marius Munneke and {te Velde}, {Anje A.} and Meijer, {Sybren L.} and Kees Weijer and Hreggvidsdottir, {Hulda S.} and Heinsbroek, {Sigrid E.} and Nicolas Legrand and Buskens, {Christianne J.} and Bemelman, {Willem A.} and Mj{\"o}sberg, {Jenny M.} and Hergen Spits",
year = "2013",
doi = "10.1038/ni.2534",
language = "English",
volume = "14",
pages = "221--229",
journal = "Nature immunology",
issn = "1529-2908",
publisher = "Nature Publishing Group",
number = "3",

}

RIS

TY - JOUR

T1 - Human type 1 innate lymphoid cells accumulate in inflamed mucosal tissues

AU - Bernink, Jochem H.

AU - Peters, Charlotte P.

AU - Munneke, Marius

AU - te Velde, Anje A.

AU - Meijer, Sybren L.

AU - Weijer, Kees

AU - Hreggvidsdottir, Hulda S.

AU - Heinsbroek, Sigrid E.

AU - Legrand, Nicolas

AU - Buskens, Christianne J.

AU - Bemelman, Willem A.

AU - Mjösberg, Jenny M.

AU - Spits, Hergen

PY - 2013

Y1 - 2013

N2 - Innate lymphoid cells (ILCs) are effectors of innate immunity and regulators of tissue modeling. Recently identified ILC populations have a cytokine expression pattern that resembles that of the helper T cell subsets T(H)2, T(H)17 and T(H)22. Here we describe a distinct ILC subset similar to T(H)1 cells, which we call 'ILC1'. ILC1 cells expressed the transcription factor T-bet and responded to interleukin 12 (IL-12) by producing interferon-γ (IFN-γ). ILC1 cells were distinct from natural killer (NK) cells as they lacked perforin, granzyme B and the NK cell markers CD56, CD16 and CD94, and could develop from RORγt(+) ILC3 under the influence of IL-12. The frequency of the ILC1 subset was much higher in inflamed intestine of people with Crohn's disease, which indicated a role for these IFN-γ-producing ILC1 cells in the pathogenesis of gut mucosal inflammation

AB - Innate lymphoid cells (ILCs) are effectors of innate immunity and regulators of tissue modeling. Recently identified ILC populations have a cytokine expression pattern that resembles that of the helper T cell subsets T(H)2, T(H)17 and T(H)22. Here we describe a distinct ILC subset similar to T(H)1 cells, which we call 'ILC1'. ILC1 cells expressed the transcription factor T-bet and responded to interleukin 12 (IL-12) by producing interferon-γ (IFN-γ). ILC1 cells were distinct from natural killer (NK) cells as they lacked perforin, granzyme B and the NK cell markers CD56, CD16 and CD94, and could develop from RORγt(+) ILC3 under the influence of IL-12. The frequency of the ILC1 subset was much higher in inflamed intestine of people with Crohn's disease, which indicated a role for these IFN-γ-producing ILC1 cells in the pathogenesis of gut mucosal inflammation

U2 - 10.1038/ni.2534

DO - 10.1038/ni.2534

M3 - Article

C2 - 23334791

VL - 14

SP - 221

EP - 229

JO - Nature immunology

JF - Nature immunology

SN - 1529-2908

IS - 3

ER -

ID: 1833249