期刊
EUROPEAN JOURNAL OF IMMUNOLOGY
卷 50, 期 6, 页码 873-879出版社
WILEY
DOI: 10.1002/eji.201948456
关键词
development; IL-17; SHP; skin inflammation; gamma delta T cells
类别
资金
- Lundbeckfonden [R163-2013-15201] Funding Source: Medline
- LEO Fondet [LF16020] Funding Source: Medline
IL-17-producing gamma delta (gamma delta T17) 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 gamma delta T17 cell activation. Immune checkpoint receptors (ICRs) deliver inhibitory signals to activated lymphocytes and have been implicated as negative regulators of mouse gamma delta T17 cells. In this report, we investigated the cytokine signals that induce ICR expression on gamma delta T17 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 gamma delta T17-induced psoriasis. We found that surface expression of ICRs can be induced by cytokines; however, SHP-1 or SHP-2 could not inhibit gamma delta T17 responses. In this regard, conditional deletion of SHP-1, SHP-2, or both did no impact gamma delta T17 cell development, expansion, cytokine production, or skin pathology.
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