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T cell-intrinsic IL-1R signaling licenses effector cytokine production by memory CD4 T cells

Author

Listed:
  • Aakanksha Jain

    (University of Texas Southwestern Medical Center)

  • Ran Song

    (University of Texas Southwestern Medical Center)

  • Edward K. Wakeland

    (University of Texas Southwestern Medical Center)

  • Chandrashekhar Pasare

    (University of Texas Southwestern Medical Center
    Cincinnati Children’s Hospital Medical Center)

Abstract

Innate cytokines are critical drivers of priming and differentiation of naive CD4 T cells, but their functions in memory T cell response are largely undefined. Here we show that IL-1 acts as a licensing signal to permit effector cytokine production by pre-committed Th1 (IFN-γ), Th2 (IL-13, IL-4, and IL-5) and Th17 (IL-17A, IL-17F, and IL-22) lineage cells. This licensing function of IL-1 is conserved across effector CD4 T cells generated by diverse immunological insults. IL-1R signaling stabilizes cytokine transcripts to enable productive and rapid effector functions. We also demonstrate that successful lineage commitment does not translate into productive effector functions in the absence of IL-1R signaling. Acute abrogation of IL-1R signaling in vivo results in reduced IL-17A production by intestinal Th17 cells. These results extend the role of innate cytokines beyond CD4 T cell priming and establish IL-1 as a licensing signal for memory CD4 T cell function.

Suggested Citation

  • Aakanksha Jain & Ran Song & Edward K. Wakeland & Chandrashekhar Pasare, 2018. "T cell-intrinsic IL-1R signaling licenses effector cytokine production by memory CD4 T cells," Nature Communications, Nature, vol. 9(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-05489-7
    DOI: 10.1038/s41467-018-05489-7
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    1. S. Fiorenza & Y. Zheng & J. Purushe & T. J. Bock & J. Sarthy & D. H. Janssens & A. S. Sheih & E. L. Kimble & D. Kirchmeier & T. D. Phi & J. Gauthier & A. V. Hirayama & S. R. Riddell & Q. Wu & R. Gotta, 2024. "Histone marks identify novel transcription factors that parse CAR-T subset-of-origin, clinical potential and expansion," Nature Communications, Nature, vol. 15(1), pages 1-17, December.

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