title: Increased Tim-3 expression on peripheral lymphocytes from patients with rheumatoid arthritis negatively correlates with disease activity.
abstract: Tim-3 has been reported as an important regulatory molecule and plays a pivotal role in several autoimmunity diseases. Here, we demonstrated the increased expression of Tim-3 on peripheral CD4(+) T, CD8(+) T, NKT cells and monocytes from RA patients compared to those from healthy controls. Percentage of Tim-3(+) cells in peripheral blood mononuclear cells (PBMCs) showed an inverse correlation with disease activity score 28 (DAS28) and plasma TNF-α level. Similar negative correlations were found between disease activity and Tim-3 levels on CD4(+) T, CD8(+) T and NKT cells. Consistently, Tim-3 expression on CD3(+) T cells was further increased in patients with disease remission after treatment. Tim-3 expression on CD8(+) T and NKT cells negatively correlates with plasma TNF-α. Our results suggest that Tim-3 might participate in the proceeding of RA by its negative regulation on various T cell subsets. Tim-3 might be a potential new marker for assessing severity of RA.
authors.affiliation: Institute of Immunology, Key Laboratory for Experimental Teratology of Ministry of Education, Shandong University School of Medicine, 44# Wenhua Xi Road, Jinan, Shandong, 250012, PR China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Liu
authors.forename: Qiang
authors.initials: Q
authors.lastname: Shu
authors.forename: Lifen
authors.initials: L
authors.lastname: Gao
authors.forename: Nan
authors.initials: N
authors.lastname: Hou
authors.forename: Di
authors.initials: D
authors.lastname: Zhao
authors.forename: Xiao
authors.initials: X
authors.lastname: Liu
authors.forename: Xiaoning
authors.initials: X
authors.lastname: Zhang
authors.forename: Liyun
authors.initials: L
authors.lastname: Xu
authors.forename: Xuetian
authors.initials: X
authors.lastname: Yue
authors.forename: Faliang
authors.initials: F
authors.lastname: Zhu
authors.forename: Chun
authors.initials: C
authors.lastname: Guo
authors.forename: Xiaohong
authors.initials: X
authors.lastname: Liang
authors.forename: Chunhong
authors.initials: C
authors.lastname: Ma
mesh_terms: D000328:Adult; D000911:Antibodies, Monoclonal / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D001172:Arthritis, Rheumatoid / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology* / Q000503:physiopathology; D015415:Biomarkers / Q000378:metabolism; D015496:CD4-Positive T-Lymphocytes / Q000378:metabolism; D018414:CD8-Positive T-Lymphocytes / Q000378:metabolism; D005260:Female; D000072597:Hepatitis A Virus Cellular Receptor 2; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000378:metabolism; D008214:Lymphocytes / Q000378:metabolism*; D008297:Male; D008565:Membrane Proteins / Q000378:metabolism*; D008727:Methotrexate / Q000627:therapeutic use; D008875:Middle Aged; D009000:Monocytes / Q000378:metabolism; D055611:Natural Killer T-Cells / Q000378:metabolism; D012720:Severity of Illness Index; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D015854:Up-Regulation; D055815:Young Adult
chemical_list: D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D015415:Biomarkers; C448908:HAVCR2 protein, human; D000072597:Hepatitis A Virus Cellular Receptor 2; D008565:Membrane Proteins; D014409:Tumor Necrosis Factor-alpha; C502936:tocilizumab; D008727:Methotrexate