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

نویسندگان

  • 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
چکیده

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.

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عنوان ژورنال:
  • Immunity

دوره 38 6  شماره 

صفحات  -

تاریخ انتشار 2013