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Last update 08 May 2025

LILRB3

Last update 08 May 2025

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

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

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

HG-1205

Target

CD89 x LILRB3 x OSCAR

Mechanism

CD89 modulators [+2]

Active Org.-

Originator Org.

Human Genome Sciences, Inc.

Active Indication-

Inactive Indication

Bone Diseases [+2]

Drug Highest PhasePending

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

Literatures (Medical) associated with LILRB3

01 Jun 2025·International Journal of Cancer

Immunoglobulin‐like transcript 5 polarizes M2‐like tumor‐associated macrophages for immunosuppression in non‐small cell lung cancer

Article

Author: Wang, Shuyun ; Li, Juan ; He, Yifu ; Yang, Yang ; Xu, Huijun ; Ge, Yihui ; Zhang, Lu ; Gao, Aiqin ; Sun, Yuping ; Fu, Xuebing ; Zhang, Fang

AbstractImmune checkpoint inhibitors (ICIs) have shifted the treatment paradigm of non‐small cell lung cancer (NSCLC) over the last decade. Despite notable therapeutic advancements in responders, the response rate remains limited owing to the immunosuppressive tumor microenvironment (TME). Therefore, to improve the efficacy of ICIs, it is essential to explore alternative targets or signals that mediate immunosuppression. Immunoglobulin‐like transcript (ILT) 5 is a negative regulator of immune activation in myeloid cells. However, the expression and function of ILT5 in NSCLC remain unknown. Here, we found that ILT5 was highly expressed in tumor‐associated macrophages (TAMs) of NSCLC tissues and predicted poor patient survival. Functionally, ILT5 induces the M2‐like polarization of TAMs, which subsequently decreases the density of T cells, and increases FOXP3+T cell accumulation, leading to an immunosuppressive TME. The combination of ILT5 expression with M2‐like TAM density is a more reliable biomarker of patient survival than ILT5 expression alone. ILT5 knockout mitigates the reprogramming of TAM and T cell subsets toward immunosuppressive phenotypes and inhibits tumor growth in vivo. These findings highlight that ILT5 is a potential immunotherapeutic target and a promising prognostic biomarker for NSCLC.

01 May 2025·Nature Reviews Nephrology

Association of LILRB3 variants with kidney transplant failure in African Americans

Article

Author: Allison, Susan J

01 May 2025·Journal of Applied Genetics

Bioinformatics screening of prognostic immune-related genes in renal clear cell carcinoma

Article

Author: Zhang, Han ; Song, He ; Sun, Peiyu ; Cui, Kai

This study aims to harness bioinformatics to identify prognostic immune-related genes in clear cell renal cell carcinoma (ccRCC), focusing particularly on LILRB3. It evaluates LILRB3's expression in ccRCC, its association with patient prognosis, and its potential as a biomarker for predicting survival, thereby providing a preliminary basis for the diagnosis of ccRCC. Utilizing The Cancer Genome Atlas (TCGA) datasets and an immune gene set, we sought immune-related genes with elevated expression in ccRCC. Seventy-two normal tissue samples and 531 ccRCC samples were analyzed, and differential genes were identified with a screening criterion of fold change (FC) > 2 and P value < 0.01. Survival analysis and receiver operating characteristic (ROC) curve analysis were employed to discover genes of prognostic and diagnostic relevance to ccRCC. Pearson correlation analysis with a cutoff of |r|≥ 0.5, facilitated by cBioPortal, assessed genes co-expressed with LILRB3. The DAVID online tool conducted functional and pathway enrichment analyses for LILRB3-coexpressed genes. The TIMER and TCIA databases were utilized to explore LILRB3's influence on immune infiltration in the tumor microenvironment and its relation to key immunological checkpoints. Screening the TCGA database revealed 3719 up-regulated differential genes in ccRCC, with 355 overlapping immune-related genes. Survival analysis of these 355 genes revealed 100 with significant survival impact. ROC curve analysis pinpointed the top 10 genes, including LILRB3, with the highest diagnostic efficiency. LILRB3 emerged as an independent risk factor from the Cox risk regression model. GO and KEGG analyses linked LILRB3 to various biological processes, including chemokine signaling pathways, immunological response, antigen processing and presentation, inflammatory response, T cell co-stimulation, and signal transduction. LILRB3 significantly affected ccRCC immune infiltration and correlated positively with several immunological checkpoints, such as PD-1, LAG3, IDO1, PD-L1, CTLA4, TIM3, TIGIT, and VISTA. LILRB3 shows higher expression levels in ccRCC than in normal tissues and correlates with poor patient prognosis. Its impactful role in the immune infiltration of the RCC microenvironment suggests that LILRB3 could serve as a novel target for ccRCC treatment and prognosis, underlining its diagnostic and prognostic significance.

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LILRB3

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