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Last update 08 May 2025

CD72

Last update 08 May 2025

Basic Info

Synonyms

B-cell differentiation antigen CD72, CD72, CD72 molecule

+ [3]

Introduction

Co-receptor of B cell receptor (BCR) that plays both positive and negative roles on B-cell functions. Recognizes the Sm/ribonucleoprotein (RNP) self-antigen ligand, and coligation of CD72 and BCR inhibits BCR signaling. Mechanistically, ligand binding leads to the recruitment of PTPN6/SHP-1 to the BCR complex which is inhibitory to BCR signaling. Acts also as a ligand for CD5 and thereby plays a critical role in maintaining regulatory T and B-cell homeostasis.

Drugs associated with CD72

NbD4.13-H24 nanoCAR(UCSF)

Target

CD72

Mechanism

CD72 inhibitors

Active Org.

The University of California, San Francisco

Originator Org.

The University of California, San Francisco

Active Indication

B-Cell Malignant Neoplasm

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

T-sema3A (Bnai Zion Medical Center)

Target

CD72

Mechanism

CD72 modulators

Active Org.

Bnai Zion Medical Center [+1]

Originator Org.

Bnai Zion Medical Center

Active Indication

Immune System Diseases

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

H24 nanoCARs(San Francisco Conservatory of Music/University of California)

Target

CD72

Mechanism

CD72 inhibitors

Active Org.

San Francisco Conservatory of Music [+1]

Originator Org.

San Francisco Conservatory of Music [+1]

Active Indication

Acute Lymphoblastic Leukemia

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CD72

100 Translational Medicine associated with CD72

0 Patents (Medical) associated with CD72

361

Literatures (Medical) associated with CD72

01 Apr 2025·International Immunopharmacology

A cohort of highly activated CD99− CD72+ B cells promoting autoimmune progression in juvenile systemic lupus erythematosus

Article

Author: Xi, Ting ; Wen, Yini ; Fang, Guofeng ; Tang, Hongxia ; Wu, Yali ; Liu, Yi ; Chen, Jing

CD72 inhibits the development of systemic lupus erythematosus (SLE) by suppressing TLR7-dependent B cell responses to self-nucleic acids (NAs). The absence of CD72 promotes the progression of lupus disease. Here, we find a highly activated subset of CD99^- CD72⁺ B cells (CD72⁺ BCs) expressing elevated levels of TLR7 in juvenile SLE, which contributes to autoimmunity. Through multi-omics integrated analysis of single-cell RNA sequencing(scRNA-seq) data and bulk RNA sequencing (RNA-seq) data, we demonstrate that CD72⁺ BCs possess characteristics of both activated naïve B cells (aN) and age-associated B cells (ABCs). Concurrently, CD72⁺ BCs exhibit pronounced plasmablast-like features compared to other cellular subpopulations. We propose a plausible conclusion that CD72⁺ BCs represent a critical transitional cell population involved in the activation and subsequent plasma cell differentiation of naïve B cells and age-related B cells following exposure to self-antigens in SLE. This finding offers novel opportunities for elucidating the genesis of autoantibody-secreting cells involved in the autoimmune response processes in lupus.

01 Feb 2025·International Immunopharmacology

Soluble CD72 concurrently impairs T cell functions while enhances inflammatory response in sepsis

Article

Author: Zhang, Wei ; Liao, Xuelian ; Xiao, Fei ; Feng, Zhongxue ; Kang, Yan ; Ma, Chengyong ; Yang, Jing

BACKGROUNDSepsis is defined as multi-organ dysfunction caused by dysregulated host response to infection. This dysregulated host response includes enhanced inflammatory responses and suppressed adaptive immunity, but the molecular mechanisms behind it have not yet been elucidated. CD72, a type II transmembrane protein that is primarily expressed in B cells, was found to play an immunomodulatory role in the immune system and was associated with mortality in patients with sepsis. However, whether CD72 affects the pathogenesis of sepsis by influencing the immune response remains unclear.METHODSWe first collected peripheral blood from 40 healthy volunteers and 57 septic patients and analyzed the mRNA levels of CD72 and the expression of its soluble form sCD72 using Realtime-PCR and ELISA. We then employed the CRISPR/Cas9 system to generate CD72 knockout mice (CD72-KO) and established a cecal ligation and puncture (CLP) model to analyze the effects of CD72 gene deletion on the survival, organ injury and immune response of septic mice by Kaplan-Meier survival analysis, pathological sections and flow cytometry. We also observe the effects of excess sCD72 on survival and immune response in sepsis by injecting recombinant CD72 protein into mice. Finally, the mechanism of sCD72 affecting sepsis immunity was analyzed by fluorescence staining, confocal microscopy and flow cytometry.RESULTSWe found that when sepsis occurs, the levels of CD72 mRNA and cell surface CD72 in immune cells decrease, while the level of soluble sCD72 in the blood increases significantly. Excessive sCD72 increased sepsis mortality in a dose-dependent manner, which can bind to CD100 on the surface of T cells and enter the cytoplasm, leading to impaired T cell functions, including a decrease in CD4⁺IFN-γ⁺, CD8⁺Perforin⁺, CD8⁺GZMB⁺, and CD8⁺FASL⁺ population and an increase in inflammatory CD4⁺TNF-α⁺ population, thereby suppressing adaptive immunity while enhancing inflammatory response.CONCLUSIONThe immunosuppression of sepsis has been recognized, but the underlying mechanism has not been fully elucidated. Our study identified for the first time that sCD72 is an important mediator that cause adaptive immunosuppression during sepsis, which leads to T cell suppression by competitively binding to CD100 on the surface of T cells. Our study provides novel insights in our understanding of sepsis-related immunosuppression and may provide translational opportunities for the design of new diagnostic biomarkers and therapeutic targets for sepsis.

01 Dec 2024·Experimental Neurology

Integrative transcriptomic analysis reveals Cd72 as a novel pro-inflammatory factor in microglia following experimental ischemic stroke

Article

Author: Bai, Lei ; Cao, Chang ; Li, Xiang ; Li, Haiying ; Lu, Jinxin ; Ding, Haojie ; Shi, Xuan ; Ma, Junwei ; Liu, Yangyang

Ischemic stroke remains a leading cause of global mortality and disability, with neuroinflammation playing a critical role in determining patient outcomes. Microglia, the brain's resident immune cells, can both exacerbate neuroinflammation and neuronal damage by releasing neurotoxic mediators and engaging in excessive phagocytosis, while also aiding recovery through the production of anti-inflammatory cytokines and debris clearance. However, the molecular mechanisms governing microglial activation and polarization after ischemic stroke are not well elucidated. In this study, we combined integrative transcriptomic analyses with experimental validation in a murine model of middle cerebral artery occlusion/reperfusion (MCAO/R) to explore microglial heterogeneity and identify key regulatory factors in ischemic stroke. Bioinformatics analysis identified Cd72 as a novel pro-inflammatory modulator within ischemia-associated microglial phenotypes. We observed significant upregulation of Cd72 in microglia following MCAO/R, and selective knockdown of Cd72 using CX3CR1^Cre/ERT2 mice and Cre recombinase-dependent adeno-associated virus reduced MCAO/R-induced infarct volume, neuronal apoptosis, and neurological deficits. Furthermore, Cd72 expression in microglia was positively correlated with pro-inflammatory pathways and cytokines, including TNF-α, IL-1β, and IL-6. Knockdown of Cd72 significantly reduced these pro-inflammatory factors, highlighting its potential as a therapeutic target for mitigating inflammation in ischemic stroke. In conclusion, this study identifies Cd72 as a critical pro-inflammatory regulator in microglia following ischemic stroke, with its knockdown effectively reducing neuroinflammation and associated brain injury, highlighting Cd72 as a promising therapeutic target.

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CD72

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