RORγt+ Innate Lymphoid Cells Acquire a Proinflammatory Program upon Engagement of the Activating Receptor NKp44

Timor Glatzer; Monica Killig; Johannes Meisig; Isabelle Ommert; Merlin Luetke-Eversloh; Marina Babic; Daniela Paclik; Nils Blüthgen; Rainer Seidl; Claudia Seifarth; Jörn Gröne; Minoo Lenarz; Katharina Stölzel; Dominik Fugmann; Angel Porgador; Anja Hauser; Alexander Karlas; Chiara Romagnani

doi:10.1016/j.immuni.2013.05.013

RORγt⁺ Innate Lymphoid Cells Acquire a Proinflammatory Program upon Engagement of the Activating Receptor NKp44

Timor Glatzer, Monica Killig, Johannes Meisig, Isabelle Ommert, Merlin Luetke-Eversloh, Marina Babic, Daniela Paclik, Nils Blüthgen, Rainer Seidl, Claudia Seifarth, Jörn Gröne, Minoo Lenarz, Katharina Stölzel, Dominik Fugmann, Angel Porgador, Anja Hauser, Alexander Karlas, Chiara Romagnani

The Shraga Segal Department of Microbiology and Immunology

Research output: Contribution to journal › Article › peer-review

153 Scopus citations

Abstract

RORγt⁺ innate lymphoid cells are crucial players of innate immune responses and represent a major source of interleukin-22 (IL-22), which has an important role in mucosal homeostasis. The signals required by RORγt⁺ ILCs to express IL-22 and other cytokines have been elucidated only partially. Here we showed that RORγt⁺ ILCs can directly sense the environment by the engagement of the activating receptor NKp44. NKp44 triggering in RORγt⁺ ILCs selectively activated a coordinated proinflammatory program, including tumor necrosis factor (TNF), whereas cytokine stimulation preferentially induced IL-22 expression. However, combined engagement of NKp44 and cytokine receptors resulted in a strong synergistic effect. These data support the concept that NKp44⁺ RORγt⁺ ILCs can be activated without cytokines and are able to switch between IL-22 or TNF production, depending on the triggering stimulus.

Original language	English
Pages (from-to)	1223-1235
Number of pages	13
Journal	Immunity
Volume	38
Issue number	6
DOIs	https://doi.org/10.1016/j.immuni.2013.05.013
State	Published - 27 Jun 2013

ASJC Scopus subject areas

Immunology and Allergy
Immunology
Infectious Diseases

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Glatzer, T., Killig, M., Meisig, J., Ommert, I., Luetke-Eversloh, M., Babic, M., Paclik, D., Blüthgen, N., Seidl, R., Seifarth, C., Gröne, J., Lenarz, M., Stölzel, K., Fugmann, D., Porgador, A., Hauser, A., Karlas, A., & Romagnani, C. (2013). RORγt⁺ Innate Lymphoid Cells Acquire a Proinflammatory Program upon Engagement of the Activating Receptor NKp44. Immunity, 38(6), 1223-1235. https://doi.org/10.1016/j.immuni.2013.05.013

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title = "RORγt+ Innate Lymphoid Cells Acquire a Proinflammatory Program upon Engagement of the Activating Receptor NKp44",

abstract = "RORγt+ innate lymphoid cells are crucial players of innate immune responses and represent a major source of interleukin-22 (IL-22), which has an important role in mucosal homeostasis. The signals required by RORγt+ ILCs to express IL-22 and other cytokines have been elucidated only partially. Here we showed that RORγt+ ILCs can directly sense the environment by the engagement of the activating receptor NKp44. NKp44 triggering in RORγt+ ILCs selectively activated a coordinated proinflammatory program, including tumor necrosis factor (TNF), whereas cytokine stimulation preferentially induced IL-22 expression. However, combined engagement of NKp44 and cytokine receptors resulted in a strong synergistic effect. These data support the concept that NKp44+ RORγt+ ILCs can be activated without cytokines and are able to switch between IL-22 or TNF production, depending on the triggering stimulus.",

author = "Timor Glatzer and Monica Killig and Johannes Meisig and Isabelle Ommert and Merlin Luetke-Eversloh and Marina Babic and Daniela Paclik and Nils Bl{\"u}thgen and Rainer Seidl and Claudia Seifarth and J{\"o}rn Gr{\"o}ne and Minoo Lenarz and Katharina St{\"o}lzel and Dominik Fugmann and Angel Porgador and Anja Hauser and Alexander Karlas and Chiara Romagnani",

year = "2013",

month = jun,

day = "27",

doi = "10.1016/j.immuni.2013.05.013",

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Glatzer, T, Killig, M, Meisig, J, Ommert, I, Luetke-Eversloh, M, Babic, M, Paclik, D, Blüthgen, N, Seidl, R, Seifarth, C, Gröne, J, Lenarz, M, Stölzel, K, Fugmann, D, Porgador, A, Hauser, A, Karlas, A & Romagnani, C 2013, 'RORγt⁺ Innate Lymphoid Cells Acquire a Proinflammatory Program upon Engagement of the Activating Receptor NKp44', Immunity, vol. 38, no. 6, pp. 1223-1235. https://doi.org/10.1016/j.immuni.2013.05.013

TY - JOUR

T1 - RORγt+ Innate Lymphoid Cells Acquire a Proinflammatory Program upon Engagement of the Activating Receptor NKp44

AU - Glatzer, Timor

AU - Killig, Monica

AU - Meisig, Johannes

AU - Ommert, Isabelle

AU - Luetke-Eversloh, Merlin

AU - Babic, Marina

AU - Paclik, Daniela

AU - Blüthgen, Nils

AU - Seidl, Rainer

AU - Seifarth, Claudia

AU - Gröne, Jörn

AU - Lenarz, Minoo

AU - Stölzel, Katharina

AU - Fugmann, Dominik

AU - Porgador, Angel

AU - Hauser, Anja

AU - Karlas, Alexander

AU - Romagnani, Chiara

PY - 2013/6/27

Y1 - 2013/6/27

N2 - RORγt+ innate lymphoid cells are crucial players of innate immune responses and represent a major source of interleukin-22 (IL-22), which has an important role in mucosal homeostasis. The signals required by RORγt+ ILCs to express IL-22 and other cytokines have been elucidated only partially. Here we showed that RORγt+ ILCs can directly sense the environment by the engagement of the activating receptor NKp44. NKp44 triggering in RORγt+ ILCs selectively activated a coordinated proinflammatory program, including tumor necrosis factor (TNF), whereas cytokine stimulation preferentially induced IL-22 expression. However, combined engagement of NKp44 and cytokine receptors resulted in a strong synergistic effect. These data support the concept that NKp44+ RORγt+ ILCs can be activated without cytokines and are able to switch between IL-22 or TNF production, depending on the triggering stimulus.

AB - RORγt+ innate lymphoid cells are crucial players of innate immune responses and represent a major source of interleukin-22 (IL-22), which has an important role in mucosal homeostasis. The signals required by RORγt+ ILCs to express IL-22 and other cytokines have been elucidated only partially. Here we showed that RORγt+ ILCs can directly sense the environment by the engagement of the activating receptor NKp44. NKp44 triggering in RORγt+ ILCs selectively activated a coordinated proinflammatory program, including tumor necrosis factor (TNF), whereas cytokine stimulation preferentially induced IL-22 expression. However, combined engagement of NKp44 and cytokine receptors resulted in a strong synergistic effect. These data support the concept that NKp44+ RORγt+ ILCs can be activated without cytokines and are able to switch between IL-22 or TNF production, depending on the triggering stimulus.

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SN - 1074-7613

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JO - Immunity

JF - Immunity

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ER -

RORγt⁺ Innate Lymphoid Cells Acquire a Proinflammatory Program upon Engagement of the Activating Receptor NKp44

Abstract

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