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  • IL-7Rα glutamylation and activation of transcription factor Sall3 promote group 3 ILC development.

IL-7Rα glutamylation and activation of transcription factor Sall3 promote group 3 ILC development.

Nature communications (2017-08-11)
Benyu Liu, Buqing Ye, Xiaoxiao Zhu, Guanling Huang, Liuliu Yang, Pingping Zhu, Ying Du, Jiayi Wu, Shu Meng, Yong Tian, Zusen Fan
要旨

Group 3 innate lymphoid cells (ILC3) promote lymphoid organogenesis and potentiate immune responses against bacterial infection. However, how ILC3 cells are developed and maintained is still unclear. Here, we show that carboxypeptidase CCP2 is highly expressed in common helper-like innate lymphoid progenitors, the progenitor of innate lymphoid cells, and CCP2 deficiency increases ILC3 numbers. Interleukin-7 receptor subunit alpha (IL-7Rα) is identified as a substrate of CCP2 for deglutamylation, and IL-7Rα polyglutamylation is catalyzed by polyglutamylases TTLL4 and TTLL13 in common helper-like innate lymphoid progenitors. IL-7Rα polyglutamylation triggers STAT5 activation to initiate transcription factor Sall3 expression in common helper-like innate lymphoid progenitors, which drives ILC3 cell differentiation. Moreover, Ttll4

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Sigma-Aldrich
モノクローナル ANTI-FLAG® M1 抗体 マウス宿主抗体, clone M1, purified immunoglobulin, buffered aqueous solution
Sigma-Aldrich
MONOCLONAL ANTI-HIS TAG(モノクローナル抗HIS TAG) マウス宿主抗体, clone 6AT18, IgG fraction of antiserum, buffered aqueous solution
Sigma-Aldrich
Anti-phospho-STAT2 (pTyr690) antibody produced in rabbit, affinity isolated antibody
Sigma-Aldrich
抗SALL3 ウサギ宿主抗体, affinity isolated antibody