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

Research output: Contribution to journalArticlepeer-review

131 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 languageEnglish
Pages (from-to)1223-1235
Number of pages13
JournalImmunity
Volume38
Issue number6
DOIs
StatePublished - 27 Jun 2013
Externally publishedYes

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