Increased expression of human T-cell immunoglobulin-and mucin-domain-containing molecule-4 in peripheral blood mononuclear cells from patients with system lupus erythematosus

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 molecul...

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Veröffentlicht in:Cellular & molecular immunology 2010-03, Vol.7 (2), p.152-156
Hauptverfasser: Zhao, Peiqing, Xu, Liyun, Wang, Piming, Liang, Xiaohong, Qi, Jianni, Liu, Peng, Guo, Chun, Zhang, Lining, Ma, Chunhong, Gao, Lifen
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Sprache:eng
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Zusammenfassung: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 l igand for Tim-4) in PB MCs and serum tumor necrosis factor (TNF)-a 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-a 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.
ISSN:1672-7681
2042-0226
DOI:10.1038/cmi.2009.118