IFN-γ-producing Th1-like regulatory T cells may limit acute cellular renal allograft rejection: Paradoxical post-transplantation effects of IFN-γ
Immunobiology, ISSN: 0171-2985, Vol: 222, Issue: 2, Page: 280-290
2017
- 23Citations
- 24Captures
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Metrics Details
- Citations23
- Citation Indexes23
- 23
- CrossRef16
- Captures24
- Readers24
- 24
Article Description
IFN-γ is a protypical proinflammatory cytokine that plays a central role in inflammation and acute graft rejection. Accumulating evidence indicates that IFN-γ can exert previously unexpected immunoregulatory activities. However, little is known about the role of IFN-γ secreted by Th1-like regulatory T cells in human kidney transplantation. To determine the function of IFN-γ in acute T cell-mediated renal allograft rejection (ACR), we examined serum cytokine expression profiles in ACR patients by human cytokine multiplex immunoassay and analyzed the cellular origins of IFN-γ in peripheral blood and renal allograft biopsies from ACR cases and controls by flow cytometry and immunohistochemistry, respectively. The results showed significant reduction in serum concentrations of Th1-inducing cytokines IL-12p70 and IFN-γ as well as Th2-related cytokine IL-4 in ACR patients compared with stable controls. However, levels of several Th1-, Th2- and Th17-related cytokines, such as IL-2, TNF-α, TNF-β, IL-12 (p40), IL-10, IL-15, IL-17, IL-21, and IL-23, as well as the frequencies of Th1 and Th17 cell, did not differ between ACR cases and stable controls. Moreover, we found the levels of IFN-γ were correlated with those of the anti-inflammatory factor, IL-1 receptor antagonist (IL-1Ra) in ACR. Notably, the Th1-like Treg cell-to-Foxp3 − Th1 cell ratio was significantly lower in ACR patients compared with that in stable controls. In graft biopsies from ACR patients, Treg cells and Th1-like Treg cells were less abundant than those without ACR. Our study indicates that IFN-γ secreted from Th1-like Treg cells negatively modulates ACR.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0171298516303734; http://dx.doi.org/10.1016/j.imbio.2016.09.012; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84994493014&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/27665996; https://linkinghub.elsevier.com/retrieve/pii/S0171298516303734; https://dx.doi.org/10.1016/j.imbio.2016.09.012
Elsevier BV
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