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Platelet Factor 4 Limits Th17 Differentiation and Ischaemia–Reperfusion Injury After Liver Transplantation in Mice
Author(s) -
Guo H.,
Wang Y.,
Zhao Z.,
Shao X.
Publication year - 2015
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.12257
Subject(s) - liver transplantation , medicine , reperfusion injury , ischemia , transplantation , platelet , immunology
Liver ischaemia/reperfusion injury ( IRI ) is a serious pathologic process encountered in a number of clinical syndromes including liver transplantation, liver resection, trauma and haemorrhagic shock. Platelet factor 4 ( PF 4) was the first discovered CXC chemokine and is found in platelet granules at very high concentration. In this study, we provide strong evidence that PF 4 is involved directly in liver innate immune response against IRI by regulating Th17 differentiation. PF 4 deficiency aggravates liver IRI , as shown by higher serum alanine aminotransferase ( ALT ) levels and Suzuki scores. PF 4 deficiency promotes Th17 response with higher levels of IL ‐23, IL ‐6 and IL ‐17, which aggravates liver IRI . Furthermore, PF 4 deficiency limits suppressor of cytokine signalling 3 ( SOCS 3) expressions, and PF 4 fails to suppress expression of IL ‐17 in cells transfected with SOCS 3 Si RNA . In conclusion, PF 4 limits liver IRI through IL ‐17 inhibition via upregulation of SOCS 3.