Increased <scp>T</scp> cell immunoglobulin and mucin domain containing 4 (<scp>TIM</scp>‐4) is negatively correlated with serum concentrations of interleukin‐1<i>β</i> in type 2 diabetes

Zhao, Peiqing; Wang, Hongxing; Li, Tao; Lei, Chengbin; Xu, Xiaoyan; Wang, Wei; Liang, Xiaohong; Ma, Chao; Gao, Lifen

doi:10.1111/1753-0407.12276

Cited by 11 publications

(10 citation statements)

References 37 publications

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“…The level of Tim-4 mRNA expression in peripheral blood of patients with Type 2 diabetes mellitus was significantly increased and negatively correlated with LDL (94). The latest report found that blocking Tim-4 could aggravate atherosclerosis in ldlr −/− mice (95), and the expression of Tim-4 mRNA was increased in liver tissues of rats on a high fat diet (96).…”

Section: Chronic Metabolic Diseasementioning

confidence: 99%

Tim-4 in Health and Disease: Friend or Foe?

Liang

et al. 2020

Front. Immunol.

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T-cell immunoglobulin and mucin domain containing 4 (Tim-4) is a phosphatidylserine receptor and is selectively expressed on antigen presenting cells. Recently, Tim-4 was reported to be expressed on iNKT cells, B1 cells, and tumor cells, suggesting it has multiple biological functions. In this review, we mainly summarize the expression and regulation of Tim-4 in immune cells including T cells, macrophages, dendritic cells, NKT cells, B cells, and mast cells. The expression of Tim-4 in these cells implies that Tim-4 might participate in immune related diseases. Emerging evidence emphasizes a substantial role for Tim-4 in maintaining homeostasis by regulating various immune responses, including viral infection, allergy, autoimmunity, and tumor immunity. Here, we collectively evaluated the role of Tim-4 in health and diseases. This summary will be extremely useful to fully understand the function of Tim-4 in the pathogenesis of immune related diseases, which would provide novel clues for the diagnosis and treatment of diseases.

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Section: Chronic Metabolic Diseasementioning

confidence: 99%

Tim-4 in Health and Disease: Friend or Foe?

Liang

et al. 2020

Front. Immunol.

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“…It has been stated that TIPE2 mRNA expression was substantially declined in individuals with SLE in contrast to healthy individuals and was negatively correlated with the SLE disease activity index (SLEDAI) and myxoma resistance protein 1 (MX1) mRNA expression levels in SLE participants [17]. Research by Feng Licon firmed that TIPE2 overexpression by adeno-associated virus prompted macrophage polarization to a M2 phenotype in vitro and in vivo in the SLE mouse model and substantially diminished SLE severity [9]. Xi et al stated that TIPE2 mRNA expression was substantially diminished in PBMCs from individuals with chronic hepatitis B in contrast to healthy people, and TIPE2 expression was negatively correlated with blood levels of ALT, AST, and total bilirubin (Tbil) and with HBV load in these patients [18].…”

Section: Discussionmentioning

confidence: 99%

“…Inflammatory markers, including IL-1 β and TNF- α , are escalated in the serum and tissues of diabetics [8, 9], and TNF- α is a vital regulatory molecules of insulin resistance in T2DM; the neutralization of TNF- α might represent a strategy for combating obesity-induced insulin resistance in individuals with T2DM. In accordance with previous research, our study showed that the mRNA level of TIPE2 was negatively linked with TNF- α and IL-6 in T2DM.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of Tumor Necrosis Factor-α-Induced Protein 8-Like 2 mRNA Is Negatively Correlated with Serum Concentrations of Tumor Necrosis Factor-α and Interleukin 6 in Type 2 Diabetes Mellitus

Liu

Wang

Zhao

et al. 2017

Journal of Diabetes Research

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Background Tumor necrosis factor-α-induced protein 8-like 2 (TIPE2 or TNFAIP8L2) is a negative regulator of natural and adaptive immunity. The role of TIPE2 in type 2 diabetes mellitus (T2DM) remains unknown, although TIPE2 plays key roles in preserving inflammatory homeostasis. Methods TIPE2 expression was measured by Western blotting and real-time polymerase chain reaction (RT-PCR) in peripheral blood mononuclear cells (PBMCs) isolated from T2DM patients and healthy controls, and tumor necrosis factor-α (TNF-α), high-sensitivity C-reactive protein (hsCRP), interleukin 6 (IL-6), and other related biometabolic parameters were detected using a nephelometer or by ELISA. Differentiated THP-1 cells were exposed to siTIPE2 and TIPE2 adenovirus. Results TIPE2 was significantly increased in PBMCs from T2DM patients compared with those from healthy controls and was negatively correlated with serum TNF-α, IL-6, and hsCRP concentrations but positively correlated with HbA1c and LDL-C in T2DM patients. High glucose treatment (50 mmol/L) can upregulate the expression of TIPE2 and cytokine secretion in differentiated THP-1 cells. siTIPE2 infection exacerbated the increased TNF-α and IL-6 concentrations in differentiated THP-1 cells under high glucose conditions (50 mmol/L), while infection with TIPE2 adenovirus reversed the increased TNF-α concentration. Conclusions The present study indicates that TIPE2 may participate in T2DM by regulating TNF-α production.

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“…16,17 Moreover, we observed increased Tim-4 expression on PBMCs from systemic lupus erythematosus 22 and type 2 diabetes patients. 23 It therefore appears that the potential role of Tim-4 is to downregulate the innate immune system, particularly macrophages, in order to decrease excessive inflammatory reactions. Recently, we identify Tim-4 as a critical regulator of LPS-induced macrophage activation by inhibiting NO production in vitro.…”

Section: Discussionmentioning

confidence: 99%

Tim-4 protects mice against lipopolysaccharide-induced endotoxic shock by suppressing the NF-κB signaling pathway

Zhao

et al. 2016

Laboratory Investigation

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Endotoxic shock is the primary cause of morbidity and mortality in hospital patients, creating an urgent need to explore the mechanisms involved in sepsis. Our previous studies showed that T-cell immunoglobulin- and mucin-domain-containing molecule-4 (Tim-4) attenuated the inflammatory response through regulating the functions of macrophages. However, the mechanism by which Tim-4 does this has not been fully elucidated. In this study, we found that Tim-4 expression was increased in lipopolysaccharide (LPS)-induced endotoxic shock. Interestingly, the survival rate of mice in the Tim-4 overexpression group was higher than that of the control group after LPS administration. To investigate the function of Tim-4 in LPS-induced inflammation, we further demonstrated that Tim-4 attenuated LPS-induced endotoxic shock by inhibiting cytokine production by macrophages. Blocking expression of Tim-4 and nuclear factor-kappa B (NF-κB) signal inhibition showed that Tim-4 inhibited cytokine production via NF-κB signaling pathway. This study indicates that Tim-4 may exert its immune modulation by regulating inflammatory factor secretion and might act as a novel potential target for inflammatory diseases, especially endotoxic shock.

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

Abstract: The results of the present study indicate that TIM-4 contributes, at least in part, to the pathogenesis of T2D, possibly by regulating IL-1β.

Cited by 11 publications

References 37 publications

Tim-4 in Health and Disease: Friend or Foe?

Tim-4 in Health and Disease: Friend or Foe?

Upregulation of Tumor Necrosis Factor-α-Induced Protein 8-Like 2 mRNA Is Negatively Correlated with Serum Concentrations of Tumor Necrosis Factor-α and Interleukin 6 in Type 2 Diabetes Mellitus

Tim-4 protects mice against lipopolysaccharide-induced endotoxic shock by suppressing the NF-κB signaling pathway

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