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
N1 - Funding Information:
We thank Toralf Kaiser and Jenny Kirsch for cell sorting, Andreas Grützkau for discussion about the microarrays, Heidi Schliemann for excellent technical assistance, Andrey Kruglov and Ofer Mandelboim for sharing reagents and helpful discussion, and Simon Fillatreau and Jens Geginat for critical reading of the manuscript and discussion. This work was supported by the Deutsche Forschungsgemeinschaft (DFG) SFB 633 and SFB 650 (to C.R.).
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.
UR - http://www.scopus.com/inward/record.url?scp=84879602800&partnerID=8YFLogxK
U2 - 10.1016/j.immuni.2013.05.013
DO - 10.1016/j.immuni.2013.05.013
M3 - Article
AN - SCOPUS:84879602800
VL - 38
SP - 1223
EP - 1235
JO - Immunity
JF - Immunity
SN - 1074-7613
IS - 6
ER -
