Open AccessIncreased expression of human T-cell immunoglobulin- and mucin-domain-containing molecule-4 in peripheral blood mononuclear cells from patients with system lupus erythematosus
Author(s) -
Peiqing Zhao,
Lixiang Xu,
Piming Wang,
Xiaohong Liang,
Jianni Qi,
Peng Liu,
Chun Guo,
Lining Zhang,
Chao Ma,
Lifen Gao
Publication year - 2010
Publication title -
cellular and molecular immunology/cellular and molecular immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.5
H-Index - 81
eISSN - 2042-0226
pISSN - 1672-7681
DOI - 10.1038/cmi.2009.118
Subject(s) - peripheral blood mononuclear cell , immunology , antibody , pathogenesis , immune system , tumor necrosis factor alpha , innate immune system , mucin , acquired immune system , medicine , biology , pathology , biochemistry , in vitro
Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease. Innate and adaptive immunity cooperatively contribute to the development of SLE. Antigen-presenting cells (APCs) have been suggested to link innate and adaptive immunity. T-cell immunoglobulin- and mucin-domain-containing molecule-4 (Tim-4; also known as Timd4), expressed primarily on the surface of APCs, is a member of the TIM family, a recently described group of molecules that have received much attention as potential regulators of the immune system. In this study, we used quantitative real-time reverse transcription-polymerase chain reaction to examine the mRNA expression of Tim-4 in peripheral blood mononuclear cells (PBMCs) from SLE patients and further analyzed the correlation between the expression of Tim-4 and Tim-1 (a potential ligand for Tim-4) in PBMCs and serum tumor necrosis factor (TNF)-alpha levels. The results showed that Tim-4 mRNA expression in PBMCs was significantly higher in SLE patients than in healthy controls, especially those patients in the active phase of disease. Moreover, Tim-4 mRNA levels were closely correlated with Tim-1 mRNA levels in PBMCs and with serum TNF-alpha levels in SLE patients but not in the control group. Taken together, these results demonstrate that Tim-4 may be involved in the pathogenesis of SLE.