title: Increased T cell immunoglobulin and mucin domain 3 positively correlate with systemic IL-17 and TNF-α level in the acute phase of ischemic stroke.
abstract: Tim-3 has been linked to several inflammatory diseases by regulation on both adaptive and innate immunities. Here, we assessed the augmented expression of Tim-3 in brain tissue of ischemia-reperfusion mice and PBMCs of ischemic stroke (IS) patients. The augmented expression of Tim-3 significantly correlated with abnormal lipid levels. In vitro studies showed that plasma from ischemic stroke patients induced Tim-3 expression in THP-1 cells. More importantly, our results revealed a significant correlation of Tim-3 expression on CD4(+) T cells with systemic IL-17 in patients with ischemic stroke. Consistently, we also found a positive correlation of Tim-3 expression on CD14(+) monocytes and serum TNF-α in IS patients. Collectively, augmented expression of Tim-3 may play an important role in the pathogenesis of ischemic stroke by regulation of proinflammatory cytokines. Further studies will give us new insights on the pathogenesis of ischemic stroke and potentially provide a new target at the medical therapy.
authors.affiliation: Key Laboratory for Experimental Teratology of the Ministry of Education and Institute of Immunology, Shandong University School of Medicine, 44# Wenhua Xi Road, Jinan, Shandong, 250012, People's Republic of China.
authors.forename: Di
authors.initials: D
authors.lastname: Zhao
authors.forename: Nan
authors.initials: N
authors.lastname: Hou
authors.forename: Min
authors.initials: M
authors.lastname: Cui
authors.forename: Ying
authors.initials: Y
authors.lastname: Liu
authors.forename: Xiaohong
authors.initials: X
authors.lastname: Liang
authors.forename: Xuewei
authors.initials: X
authors.lastname: Zhuang
authors.forename: Yuanyuan
authors.initials: Y
authors.lastname: Zhang
authors.forename: Lining
authors.initials: L
authors.lastname: Zhang
authors.forename: Deling
authors.initials: D
authors.lastname: Yin
authors.forename: Lifen
authors.initials: L
authors.lastname: Gao
authors.forename: Yun
authors.initials: Y
authors.lastname: Zhang
authors.forename: Chunhong
authors.initials: C
authors.lastname: Ma
mesh_terms: D000208:Acute Disease; D000368:Aged; D000818:Animals; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology / Q000378:metabolism; D002460:Cell Line; D016207:Cytokines / Q000096:biosynthesis / Q000378:metabolism; D005260:Female; D000072597:Hepatitis A Virus Cellular Receptor 2; D006801:Humans; D020381:Interleukin-17 / Q000097:blood*; D007511:Ischemia; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D018950:Lipopolysaccharide Receptors / Q000096:biosynthesis; D008297:Male; D008565:Membrane Proteins / Q000096:biosynthesis / Q000097:blood*; D051379:Mice; D008810:Mice, Inbred C57BL; D008875:Middle Aged; D015427:Reperfusion Injury; D020521:Stroke / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood*
chemical_list: D016207:Cytokines; C448908:HAVCR2 protein, human; D000072597:Hepatitis A Virus Cellular Receptor 2; D020381:Interleukin-17; D018950:Lipopolysaccharide Receptors; D008565:Membrane Proteins; D014409:Tumor Necrosis Factor-alpha