Last update 01 Nov 2024

LILRB3

Last update 01 Nov 2024

Basic Info

Synonyms

CD85 antigen-like family member A, CD85a, HL9

+ [12]

Introduction

May act as receptor for class I MHC antigens. Becomes activated upon coligation of LILRB3 and immune receptors, such as FCGR2B and the B-cell receptor. Down-regulates antigen-induced B-cell activation by recruiting phosphatases to its immunoreceptor tyrosine-based inhibitor motifs (ITIM).

Drugs associated with LILRB3

Anti-LILRB3 antagonistic antibody (University of Texas Southwestern Medical Center)

Target

LILRB3

Mechanism

LILRB3 inhibitors

Active Org.

The University of Texas Southwestern Medical Center

Originator Org.

The University of Texas Southwestern Medical Center

Active Indication

Solid tumor

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

LITCHI-7

Target

LILRB1 x LILRB2 x LILRB3

Mechanism

LILRB1 inhibitors [+2]

Active Org.

AbbVie Biotherapeutics, Inc.

Originator Org.

AbbVie Biotherapeutics, Inc.

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

TRX-585

Target

LILRB3

Mechanism

LILRB3 modulators

Active Org.

Tolerx, Inc.

Originator Org.

Tolerx, Inc.

Active Indication

Neoplasms [+1]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with LILRB3

100 Translational Medicine associated with LILRB3

0 Patents (Medical) associated with LILRB3

101

Literatures (Medical) associated with LILRB3

01 Sep 2024·Free Radical Biology and Medicine

Cannabidiol mitigates radiation-induced intestine ferroptosis via facilitating the heterodimerization of RUNX3 with CBFβ thereby promoting transactivation of GPX4

Article

Author: Shen, Pan ; Ao, Ting ; Wang, Ningning ; Liao, Zebin ; Quzhuo, Renzeng ; Hu, Changkun ; Gao, Yue ; Wu, Zekun ; Huang, Yijian ; Luo, Lin ; Zhang, Liangliang ; Huang, Congshu ; Li, Gaofu ; Tian, Lishan ; Huangfu, Chaoji

Radiation enteritis remains a major challenge for radiotherapy against abdominal and pelvic malignancies. Nevertheless, there is no approved effective therapy to alleviate irradiation (IR)-induced gastrointestinal (GI) toxicity. In the current study, Cannabidiol (CBD) was found to mitigate intestinal injury by GPX4-mediated ferroptosis resistance upon IR exposure. RNA-sequencing was employed to investigate the underlying mechanism involved in the radio-protective effect of CBD, wherein runt-related transcription factor 3 (RUNX3) and its target genes were changed significantly. Further experiment showed that the transactivation of GPX4 triggered by the direct binding of RUNX3 to its promoter region, or by stimulating the transcriptional activity of NF-κB via RUNX3-mediated LILRB3 upregulation was critical for the anti-ferroptotic effect of CBD upon IR injury. Specially, CBD was demonstrated to be a molecular glue skeleton facilitating the heterodimerization of RUNX3 with its transcriptional chaperone core-biding factor β (CBFβ) thereby promoting their nuclear localization and the subsequent transactivation of GPX4 and LILRB3. In short, our study provides an alternative strategy to counteract IR-induced enteritis during the radiotherapy on abdominal/pelvic neoplasms.

04 Mar 2024·Cancer Immunology Research

LILRB3 Supports Immunosuppressive Activity of Myeloid Cells and Tumor Development

Article

Author: Zhang, Cheng Cheng ; Huang, Ryan ; John, Samuel ; Wu, Guojin ; Chen, Heyu ; Xie, Jingjing ; Zhang, Chengcheng ; Lewis, Cheryl ; Deng, Mi ; He, Yubo ; Yang, Xing ; Homsi, Jade ; An, Zhiqiang ; Gui, Xun ; Smith, Caroline ; Xiong, Wei ; Kim, Jaehyup ; Lou, Qi ; Liu, Xiaoye ; Zhang, Ningyan ; Deng, Hui

AbstractThe existing T cell–centered immune checkpoint blockade therapies have been successful in treating some but not all patients with cancer. Immunosuppressive myeloid cells, including myeloid-derived suppressor cells (MDSC), that inhibit antitumor immunity and support multiple steps of tumor development are recognized as one of the major obstacles in cancer treatment. Leukocyte Ig-like receptor subfamily B3 (LILRB3), an immune inhibitory receptor containing tyrosine-based inhibitory motifs (ITIM), is expressed solely on myeloid cells. However, it is unknown whether LILRB3 is a critical checkpoint receptor in regulating the activity of immunosuppressive myeloid cells, and whether LILRB3 signaling can be blocked to activate the immune system to treat solid tumors. Here, we report that galectin-4 and galectin-7 induce activation of LILRB3 and that LILRB3 is functionally expressed on immunosuppressive myeloid cells. In some samples from patients with solid cancers, blockade of LILRB3 signaling by an antagonistic antibody inhibited the activity of immunosuppressive myeloid cells. Anti-LILRB3 also impeded tumor development in myeloid-specific LILRB3 transgenic mice through a T cell–dependent manner. LILRB3 blockade may prove to be a novel approach for immunotherapy of solid cancers.

05 Jan 2024·Mediators of Inflammation

PLCG2 and IFNAR1: The Potential Biomarkers Mediated by Immune Infiltration and Osteoclast Differentiation of Ankylosing Spondylitis in the Peripheral Blood

Article

Author: Yin, Peng ; Hai, Yong ; Han, Bo ; Xie, Qiaobo ; Qu, Xianjun ; Liang, Weishi

Objectives. Ankylosing spondylitis (AS) is a chronic inflammatory rheumatic disease characterized by chronic spinal inflammation, arthritis, gut inflammation, and enthesitis. We aimed to identify the key biomarkers related to immune infiltration and osteoclast differentiation in the pathological process of AS by bioinformatic methods. Methods. GSE25101 from the Gene Expression Omnibus was used to obtain AS-associated microarray datasets. We performed bioinformatics analysis using R software to validate different expression levels. The purpose of the GO and KEGG enrichment analyses of DEGs was to exclude key genes. Using weighted correlation network analysis (WGCNA), we examined all expression profile data and identified differentially expressed genes. The objective was to investigate the interaction between genetic and clinical features and to identify the essential relationships underlying coexpression modules. The CIBERSORT method was used to make a comparison of the immune infiltration in whole blood between the AS group and the control group. The WGCNA R program from Bioconductor was used to identify hub genes. RNA extraction reverse transcription and quantitative polymerase chain reaction were conducted in the peripheral blood collected from six AS patients and six health volunteers matched by age and sex. Results. 125 DEGs were identified, consisting of 36 upregulated and 89 downregulated genes that are involved in the cell cycle and replication processes. In the WGCNA, modules of MCODE with different algorithms were used to find 33 key genes that were related to each other in a strong way. Immune infiltration analysis found that naive CD4+ T cells and monocytes may be involved in the process of AS. PLCG2 and IFNAR1 genes were obtained by screening genes meeting the conditions of immune cell infiltration and osteoclast differentiation in AS patients among IGF2R, GRN, SH2D1A, LILRB3, IFNAR1, PLCG2, and TNFRSF1B. The results demonstrated that the levels of PLCG2 mRNA expression in AS were considerably higher than those in healthy individuals (

P = 0.003

). IFNAR1 mRNA expression levels were considerably lower in AS than in healthy individuals (

P < 0.0001

). Conclusions. Dysregulation of PLCG2 and IFNAR1 are key factors in disease occurrence and development of AS through regulating immune infiltration and osteoclast differentiation. Explaining the differences in immune infiltration and osteoclast differentiation between AS and normal samples will contribute to understanding the development of spondyloarthritis.

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LILRB3

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