C-type lectin Ocilrp2/Clec2i is widely expressed in dendritic cells, lymphokine-activated killer cells and activated T cells. Previous studies have shown that Ocilrp2 is an important regulator in the activation of T cells and NK cells. However, the role of Ocilrp2 in the inflammatory responses by activated macrophages is currently unknown. This study investigated the expression of inflammatory cytokines in LPS-induced macrophages from primary peritoneal macrophages silenced by specific siRNA target Ocilrp2. Ocilrp2 was significantly downregulated in macrophages NF-κB and pathways upon LPS stimuli or VSV infection. Silencing Ocilrp2 resulted in the increased expression of IL-6 in LPS-stimulated peritoneal macrophages and mice. Moreover, IL-6 expression was reduced in LPS-induced Ocilrp2 over-expressing iBMDM cells. Furthermore, we found that Ocilrp2-related Syk activation is responsible for expressing inflammatory cytokines in LPS-stimulated macrophages. Silencing Ocilrp2 significantly promotes the binding of Syk to Dap12. Altogether, we identified the Ocilrp2 as a critical role in the TLR4 signaling pathway and inflammatory macrophages' immune regulation, and added mechanistic insights into the crosstalk between TLR and Syk signaling.
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| http://dx.doi.org/10.3389/fimmu.2022.984520 | DOI Listing |
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Mouse Ocilrp2/Clec2i negatively regulates LPS-mediated IL-6 production by blocking Dap12-Syk interaction in macrophage.
Front Immunol
October 2022
Joint National Laboratory for Antibody Drug Engineering, The First Affiliated Hospital, School of Medicine, Henan University, Kaifeng, China.
C-type lectin Ocilrp2/Clec2i is widely expressed in dendritic cells, lymphokine-activated killer cells and activated T cells. Previous studies have shown that Ocilrp2 is an important regulator in the activation of T cells and NK cells. However, the role of Ocilrp2 in the inflammatory responses by activated macrophages is currently unknown.
View Article and Find Full Text PDFThe C-type lectin OCILRP2 costimulates EL4 T cell activation via the DAP12-Raf-MAP kinase pathway.
PLoS One
January 2016
Henan Engineering Lab of Antibody Medicine, Key Laboratory of Cellular and Molecular Immunology, Medical College of Henan University, Kaifeng 475004, China.
OCILRP2 is a typical Type-II transmembrane protein that is selectively expressed in activated T lymphocytes, dendritic cells, and B cells and functions as a novel co-stimulator of T cell activation. However, the signaling pathways underlying OCILRP2 in T cell activation are still not completely understood. In this study, we found that the knockdown of OCILRP2 expression with shRNA or the blockage of its activity by an anti-OCILRP2 antagonist antibody reduced CD3/CD28-costimulated EL4 T cell viability and IL-2 production, inhibit Raf1, MAPK3, and MAPK8 activation, and impair NFAT and NF-κB transcriptional activities.
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Biochem Biophys Res Commun
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Laboratory of Cellular and Molecular Immunology, Henan University School of Medicine, The New Campus, Jinming Road, Kaifeng 475004, People's Republic of China. Electronic address:
Osteoclast Inhibitory Lectin-related Protein 2 (OCILRP2) is a typical type II transmembrane protein and belongs to C-type lectin-related protein family. It is preferentially expressed in dendritic cells (DC), B lymphocytes, and activated T lymphocytes. Upon binding to its ligand, OCILRP2 can promote CD28-mediated co-stimulation and enhance T cell activation.
View Article and Find Full Text PDFSilencing OCILRP2 leads to intrinsic defects in T cells in response to antigenic stimulation.
Cell Immunol
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Division of Immunology, Department of Medicine, Weill Medical College of Cornell University, New York, NY 10021, USA.
We have previously demonstrated that OCILRP2 interaction with its ligand NKRP1f provides a co-stimulatory signal for optimal T cell proliferation and IL-2 production. Here, using RNA interference technology, we will demonstrate that silencing OCILRP2 in vivo leads to intrinsic impairment in T cell response to CD3- and CD28-cross-linking as well as antigenic stimulation. OCILRP2-silenced T cells have reduced cell proliferation and IL-2 production, which can be bypassed by PMA and ionomycin treatment.
View Article and Find Full Text PDFC-type lectin OCILRP2/Clr-g and its ligand NKRP1f costimulate T cell proliferation and IL-2 production.
Cell Immunol
March 2005
Division of Immunology, Department of Medicine, Weill Medical College of Cornell University, New York, NY 10021, USA.
We are reporting the identification of a novel C-type lectin receptor-ligand pair that is involved in T cell costimulation. The receptor, OCILRP2/Clr-g, is rapidly induced following T cell activation and maintained at a substantial level of up to 72 h. The ligand, NKRP1f, is predominantly expressed on dendritic cells (DC).
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