PD-1 regulates KLRG1+ group 2 innate lymphoid cells

Samuel Taylor, Yuefeng Huang, Grace Mallett, Chaido Stathopoulou, Tania C. Felizardo, Ming-An Su, Evelyn L. Martin, Nathaniel Zhu, Emma L. Woodward, Martina S. Elias, Jonathan Scott, Nick J Reynolds, William E. Paul, Daniel H. Fowler, Shoba Amarnath

Research output: Contribution to journalArticlepeer-review

Abstract

Group 2 innate lymphoid cells (ILC-2s) regulate immune responses to pathogens and maintain tissue homeostasis in response to cytokines. Positive regulation of ILC-2s through ICOS has been recently elucidated. We demonstrate here that PD-1 is an important negative regulator of KLRG1+ ILC-2 function in both mice and humans. Increase in KLRG1+ ILC-2 cell numbers was attributed to an intrinsic defect in PD-1 signaling, which resulted in enhanced STAT5 activation. During Nippostrongylus brasiliensis infection, a significant expansion of KLRG1+ ILC-2 subsets occurred in Pdcd1-/- mice and, upon adoptive transfer, Pdcd1-/- KLRG1+ ILC-2s significantly reduced worm burden. Furthermore, blocking PD-1 with an antibody increased KLRG1+ ILC-2 cell number and reduced disease burden. Therefore, PD-1 is required for maintaining the number, and hence function, of KLRG1+ ILC-2s.
Original languageEnglish
Pages (from-to)1663-1678
Number of pages16
JournalJ Exp Med.
Volume214
Issue number6
Publication statusPublished - 10 May 2017

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