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

IL-17-producing gamma delta (gammadeltaT17) cells are innate lymphocytes critical for antibacterial 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 gammadeltaT17 cell activation. Immune checkpoint receptors (ICRs) deliver inhibitory signals to activated lymphocytes and have been implicated as negative regulators of mouse gammadeltaT17 cells. In this report, we investigated the cytokine signals that induce ICR expression on gammadeltaT17 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 gammadeltaT17-induced psoriasis. We found that surface expression of ICRs can be induced by cytokines; however, SHP-1 or SHP-2 could not inhibit gammadeltaT17 responses. In this regard, conditional deletion of SHP-1, SHP-2, or both did no impact gammadeltaT17 cell development, expansion, cytokine production, or skin pathology.