Programmed death (PD)-1 attenuates macrophage activation and brain inflammation via regulation of fibrinogen-like protein 2 (Fgl-2) after intracerebral hemorrhage in mice

Highlights • ICH promoted PD-1 expression of macrophage and enhanced inflammatory cytokines and Fgl-2 concentrations. • PD-1 −/- mice exhibited significantly higher expression of the inflammatory cytokines. • Manipulation of PD-1 might be a promising therapeutical target in ICH.

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Bibliographische Detailangaben
Veröffentlicht in:	Immunology letters 2016-11, Vol.179, p.114-121
Hauptverfasser:	Yuan, Bangqing, Huang, Shaokuan, Gong, Shuangfeng, Wang, Feihong, Lin, Li, Su, Tonggang, Sheng, Haochao, Shi, Hui, Ma, Kunlong, Yang, Zhao
Format:	Artikel
Sprache:	eng
Schlagworte:	Allergy and Immunology Animals Cerebral Hemorrhage - complications Cerebral Hemorrhage - etiology Cytokines - metabolism Disease Models, Animal Encephalitis - etiology Encephalitis - metabolism Encephalitis - pathology Fgl-2 Fibrinogen - genetics Fibrinogen - metabolism Gene Expression ICH Immunohistochemistry Inflammation Inflammation Mediators - metabolism Macrophage Macrophage Activation - immunology Macrophages - immunology Macrophages - metabolism Mice Mice, Knockout PD-1 Programmed Cell Death 1 Receptor - genetics Programmed Cell Death 1 Receptor - metabolism
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Beschreibung
Zusammenfassung:	Highlights • ICH promoted PD-1 expression of macrophage and enhanced inflammatory cytokines and Fgl-2 concentrations. • PD-1 −/- mice exhibited significantly higher expression of the inflammatory cytokines. • Manipulation of PD-1 might be a promising therapeutical target in ICH.
ISSN:	0165-2478 1879-0542
DOI:	10.1016/j.imlet.2016.10.001