The immune checkpoint receptor associated phosphatases SHP-1 and SHP-2 are not required for γδT17 cell development, activation or skin inflammation

Darshana Dattatraya Kadekar*, Rasmus Agerholm*, Monica Torrellas Viñals, John Atef Micheal Baky Rizk, Vasileios Bekiaris

*Corresponding author for this work

Research output: Contribution to journalJournal articleResearchpeer-review

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Abstract

Interleukin(IL)-17 producing gamma delta (γδT17) cells are innate lymphocytes critical for anti-bacterial protection at barrier surfaces such as the skin but also highly pathogenic during inflammation. It is therefore important to understand the cellular and molecular mechanisms that could counter-balance overt γδT17 cell activation. Immune checkpoint receptors (ICRs) deliver inhibitory signals to activated lymphocytes and have been implicated as negative regulators of mouse γδT17 cells. In this report we investigated the cytokine signals that induce ICR expression on γδT17 cells and studied the in vivo role of the Src-homology-2 phosphatases 1 and 2 (SHP-1 and SHP-2) in the context of γδT17-induced psoriasis. We found that surface expression of ICRs can be induced by cytokines, however, SHP-1 or SHP-2 could not inhibit γδT17 responses. In this regard, conditional deletion of SHP-1, SHP-2 or both did no impact γδT17 cell development, expansion, cytokine production or skin pathology. This article is protected by copyright.
Original languageEnglish
JournalEuropean Journal of Immunology
Volume50
Issue number6
Pages (from-to)873-879
ISSN0014-2980
DOIs
Publication statusPublished - 2020

Keywords

  • Development
  • IL-17
  • SHP
  • Skin inflammation
  • γδ T cells

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