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Immunity. 2013 Jun 27;38(6):1223-35. doi: 10.1016/j.immuni.2013.05.013. Epub 2013 Jun 20.

RORγt⁺ innate lymphoid cells acquire a proinflammatory program upon engagement of the activating receptor NKp44.

Author information

1
Innate Immunity, Deutsches Rheuma-Forschungszentrum-Leibniz-Gemeinschaft, 10117 Berlin, Germany.

Abstract

RORγt⁺ innate lymphoid cells (ILCs) 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.

PMID:
23791642
DOI:
10.1016/j.immuni.2013.05.013
[Indexed for MEDLINE]
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