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Inhibition of T cell activation and function by the CIN85 adaptor protein

ABSTRACT: CIN85 is ubiquitously expressed adaptor protein. In T cells, CIN85 is recruited to the TCR signaling complex and inhibit TCR signaling. To reveal the molecular function of CIN85-mediated inhibition, we performed Flag-CIN85 (CIN85dA) immuno-precipitation and identified the binding proteins. As a negative control, we used deletion mutant of CIN85 (CIN85PR).

ORGANISM(S): Mus Musculus (mouse)

SUBMITTER: Takashi Saito

PROVIDER: PXD012369 | JPOST Repository | Wed Jan 16 00:00:00 GMT 2019

REPOSITORIES: jPOST

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Inhibition of T cell activation and function by the adaptor protein CIN85.

Kong Mei Suen MS Hashimoto-Tane Akiko A Kawashima Yusuke Y Sakuma Machie M Yokosuka Tadashi T Kometani Kohei K Onishi Reiko R Carpino Nick N Ohara Osamu O Kurosaki Tomohiro T Phua Kia Kien KK Saito Takashi T

Science signaling 20190205 567

T cell activation is initiated by signaling molecules downstream of the T cell receptor (TCR) that are organized by adaptor proteins. CIN85 (Cbl-interacting protein of 85 kDa) is one such adaptor protein. Here, we showed that CIN85 limited T cell responses to TCR stimulation. Compared to activated wild-type (WT) T cells, those that lacked CIN85 produced more IL-2 and exhibited greater proliferation. After stimulation of WT T cells with their cognate antigen, CIN85 was recruited to the TCR signal ...[more]

PMID: 30723173

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Project description:Recent studies have reported that glycosphingolipids (GSL) might be involved in obesity induced insulin resistance. Those reports suggested that inhibition of GSL biosynthesis in animals ameliorated insulin sensitivity accompanied with improved glycemic control leading to decreased liver steatosis in obese mice. In addition, GSL depletion altered hepatic secretory function. In those studies, ubiquitously acting inhibitors for GSL-biosynthesis have been used to inhibit function of the enzyme Ugcg (UDP-glucose:ceramide glucosyltransferase), catalyzing the first step of the glucosylceramide based GSL-synthesis pathway. In the present study, a genetic approach for GSL deletion in hepatocytes was chosen to achieve full inhibition of GSL synthesis and to prevent possible adverse effects caused by Ugcg-inhibitors. Using the Cre/loxP system under control of the albumin promoter, GSL biosynthesis in hepatocytes and their release into the plasma could be effectively blocked. Deletion of GSL in hepatocytes did not change quantity of bile excretion through the biliary duct. Total bile salt content in bile-, feces- and plasma from mutant mice showed no difference as compared to control animals. Cholesterol concentration in liver-, bile-, feces- and plasma-samples remained unaffected. Lipoprotein concentration in plasma-samples in mutant animals reached similar levels as in their control littermates. No alteration in glucose tolerance after intraperitoneal application of glucose and insulin appeared in mutant animals. A preventive effect of GSL-deficiency on development of liver steatosis after high fat diet feeding could not be observed. Conclusion: The data suggest that GSL in hepatocytes are not essential for sterol, glucose and lipoprotein metabolism and do not prevent high fat diet-induced liver steatosis, indicating that Ugcg inhibitors exert their effect on hepatocytes either independently of GSL or mediated by other (liver) cell types. Comparison of wildtype mouse liver function versus Ugcg-deficient

Dataset Information

Inhibition of T cell activation and function by the CIN85 adaptor protein

Publications

Inhibition of T cell activation and function by the adaptor protein CIN85.

Similar Datasets

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