Joulia lab - T helper cell-licensed mast cells promote inflammatory

Journal article

E. Leveque, Régis Joulia, Camille Petitfils, Xavier Mas-Orea, Gaëlle Payros, C. Laurent, Nicolas Gaudenzio, G. Dietrich, S. Valitutti, N. Cenac, E. Espinosa
bioRxiv, 2021

Semantic Scholar DOI

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APA Click to copy
Leveque, E., Joulia, R., Petitfils, C., Mas-Orea, X., Payros, G., Laurent, C., … Espinosa, E. (2021). T helper cell-licensed mast cells promote inflammatory Th17 cells. BioRxiv.

Chicago/Turabian Click to copy
Leveque, E., Régis Joulia, Camille Petitfils, Xavier Mas-Orea, Gaëlle Payros, C. Laurent, Nicolas Gaudenzio, et al. “T Helper Cell-Licensed Mast Cells Promote Inflammatory Th17 Cells.” bioRxiv (2021).

MLA Click to copy
Leveque, E., et al. “T Helper Cell-Licensed Mast Cells Promote Inflammatory Th17 Cells.” BioRxiv, 2021.

BibTeX Click to copy

@article{e2021a,
  title = {T helper cell-licensed mast cells promote inflammatory Th17 cells},
  year = {2021},
  journal = {bioRxiv},
  author = {Leveque, E. and Joulia, Régis and Petitfils, Camille and Mas-Orea, Xavier and Payros, Gaëlle and Laurent, C. and Gaudenzio, Nicolas and Dietrich, G. and Valitutti, S. and Cenac, N. and Espinosa, E.}
}

Abstract

CD4+ T helper cells (Th) infiltrate sites of inflammation and orchestrate the immune response by instructing local leukocytes. Mast cells (MCs) are tissue sentinel cells particularly abundant in skin and mucosa. Here, we analyzed the interplay between human MCs and Th cells and, through the application of RNAseq and functional assays, showed that Th cells induced a specific transcriptomic program in helped MCs (named here MCTH) driving them toward an inflammatory phenotype. The gene signature of MCTH indicated that MCs helped by Th cell acquired in turn the capacity to regulate effector T cell response through wide-range of soluble and membrane ligands. Accordingly, we showed that MCTH promoted Th17 cells and notably an inflammatory subset of Th17, producing both IFN-γ and GM-CSF, through a PGE2 and IL-1β axis. Our findings demonstrate that activated effector/memory CD4+ T cells activate and instruct resting MCs toward a specific differentiated pro-inflammatory phenotype endowed with the capacity to speak back to effector T cells and to mold their functions.