Increased T cell immunoglobulin and mucin domain containing 4 (TIM‐4) is negatively correlated with serum concentrations of interleukin‐1β in type 2 diabetes. (9th April 2015)

• Record Type: Journal Article
• Authors: Zhao, Peiqing; Wang, Hongxing; Li, Tao; Lei, Chengbin; Xu, Xiaoyan; Wang, Wei; Liang, Xiaohong; Ma, Chunhong; Gao, Lifen
• Is Part Of: Journal of diabetes. Volume 8:Number 2(2016:Mar.)
• Page Start: 199
• Page End: 205
• Publication Date: 2015-04-09
• Subjects: interleukin‐1β -- T cell immunoglobulin and mucin domain containing 4 (TIM‐4) -- type 2 diabetes; IL‐1β -- TIM‐4 -- 2型糖尿病; Diabetes -- Periodicals; 618.3646005
• DOI: 10.1111/1753-0407.12276
• Languages: English
• ISSNs: 1753-0393

Abstract

Abstract: Background: T cell immunoglobulin and mucin domain containing 4 (TIM‐4), a novel immune regulator, is selectively expressed on antigen‐presenting cells, especially macrophages and mature dendritic cells. Although TIM‐4 plays key roles in mutiple immune diseases, whether it is involved in type 2 diabetes mellitus (T2D) remains unknown. The aim of the present study was to investigate the expression of TIM‐4 in T2D and determine its significance in disease progression. Methods: Peripheral blood mononuclear cells (PBMC) were isolated from T2D patients and healthy controls to measure TIM‐4 mRNA expression by real‐time polymerase chain reaction (PCR), and sera were collected to determine interleukin (IL)‐1 β concentrations and other clinical indicators (high‐sensitivity C‐reactive protein [hsCRP], total cholesterol, low‐density lipoprotein cholesterol [LDL‐C], high‐density lipoprotein cholesterol, triglyceride, fasting glucose, HbA1c, aspartate aminotransferase, and alanine aminotransferase). Results: Expression of TIM‐4 mRNA was increased significantly in PBMCs from T2D patients compared with healthy controls. There was a positive correlation between TIM‐4 mRNA expression and serum concentrations of hsCRP. However, there was a negative correlation between TIM‐4 mRNA expression and IL‐1 β concentrations, indicating the potential role for TIM‐4 to negatively regulate IL‐1 β production. In addition, TIM‐4 mRNA expression was negatively correlated with lowLDL‐C, and there was a tendency for a negative relationship between TIM‐4 mRNA expression and HbA1c. Conclusions: The results of the present study indicate that TIM‐4 contributes, at least in part, to the pathogenesis of T2D, possibly by regulating IL‐1 β .