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In Activated Murine Mast Cells, NFATc2 Is Critical for the Production of Autocrine IL-3, Thereby Promoting the Expression of IL-9.

Abstract
IL-9 has lent its numerical designation to the Th9 subset of CD4+ Th cells, although it is also produced by additional cell types, including mast cells. It is a pleiotropic cytokine involved in allergic reactions, parasitic infections, autoimmune inflammation, and cancer immunity. In this article, we provide evidence that NFATc2 has contradictory functions in the expression of IL-9 in murine Th9 cells and bone marrow-derived mast cells (BMMC). The basis for this is our observation that the production of IL-9 in NFATc2-deficient Th9 cells is increased, whereas it is decreased in BMMC devoid of NFATc2. In addition, NFATc2 deficiency almost completely abrogates the expression of IL-3 in both cell types. However, selectively in BMMC, the production of IL-9 critically depends on autocrine IL-3 acting via the sustained activation of STAT5 on the expression of IL-9. Furthermore, we demonstrate that IL-3 acts independently and synergistically with IL-1β on the production of IL-9. Taken together, we highlight NFATc2-driven production of autocrine IL-3 as a critical and cell type-specific component for IL-9 expression in BMMC.
AuthorsFarhad Sabbaghi, Lorenz Ullner, Toszka Bohn, Jennifer Hahlbrock, Tobias Bopp, Edgar Schmitt, Matthias Klein, Michael Stassen
JournalJournal of immunology (Baltimore, Md. : 1950) (J Immunol) Vol. 206 Issue 1 Pg. 67-76 (01 01 2021) ISSN: 1550-6606 [Electronic] United States
PMID33268486 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2020 by The American Association of Immunologists, Inc.
Chemical References
  • Interleukin-3
  • Interleukin-9
  • NFATC Transcription Factors
  • STAT5 Transcription Factor
Topics
  • Animals
  • Autocrine Communication
  • Cells, Cultured
  • Feedback, Physiological
  • Interleukin-3 (metabolism)
  • Interleukin-9 (genetics, metabolism)
  • Mast Cells (immunology)
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Knockout
  • NFATC Transcription Factors (genetics, metabolism)
  • STAT5 Transcription Factor (metabolism)
  • T-Lymphocytes, Helper-Inducer (immunology)
  • Up-Regulation

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