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

Benyu Liu, Buqing Ye, Xiaoxiao Zhu, Guanling Huang, Liuliu Yang, Pingping Zhu, Ying Du, Jiayi Wu, Shu Meng, Yong Tian () and Zusen Fan ()
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Benyu Liu: Chinese Academy of Sciences
Buqing Ye: Chinese Academy of Sciences
Xiaoxiao Zhu: Chinese Academy of Sciences
Guanling Huang: Chinese Academy of Sciences
Liuliu Yang: Chinese Academy of Sciences
Pingping Zhu: Chinese Academy of Sciences
Ying Du: Chinese Academy of Sciences
Jiayi Wu: Chinese Academy of Sciences
Shu Meng: Chinese Academy of Sciences
Yong Tian: University of Chinese Academy of Sciences
Zusen Fan: Chinese Academy of Sciences

Nature Communications, 2017, vol. 8, issue 1, 1-14

Abstract: Abstract 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 −/− or Ttll13 −/− mice have reduced IL-7Rα polyglutamylation and Sall3 expression in common helper-like innate lymphoid progenitors. Importantly, mice with IL-7Rα E446A mutation have reduced Sall3 expression and ILC3 population. Thus, polyglutamylation and deglutamylation of IL-7Rα tightly controls the development and effector functions of ILC3s.

Date: 2017
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DOI: 10.1038/s41467-017-00235-x

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