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Last update 08 May 2025

CDHR3

Last update 08 May 2025

Basic Info

Synonyms

cadherin related family member 3, Cadherin-like protein 28, Cadherin-related family member 3

+ [4]

Introduction

Cadherins are calcium-dependent cell adhesion proteins. They preferentially interact with themselves in a homophilic manner in connecting cells; cadherins may thus contribute to the sorting of heterogeneous cell types. (Microbial infection) Acts as a receptor for human rhinovirus C.

Drugs associated with CDHR3

AT-005 (Arctic Therapeutics)

Target

CDHR3

Mechanism

CDHR3 inhibitors

Active Org.

Arctic Therapeutics

Originator Org.

Arctic Therapeutics

Active Indication

Asthma [+1]

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CDHR3

100 Translational Medicine associated with CDHR3

0 Patents (Medical) associated with CDHR3

Literatures (Medical) associated with CDHR3

01 Mar 2025·Antiviral Research

Transgenic mice expressing the human CDHR3 receptor: A sensitive RV-C infection model for the evaluation of vaccines and therapeutics

Article

Author: Zhang, Dongqing ; Zhang, Jun ; Fang, Mujin ; Yin, Zhichao ; Zhou, Zhenhong ; Xia, Ningshao ; Wang, Ruoxi ; Liu, Che ; Yan, Ziyang ; Zhang, Zijie ; Cheng, Tong ; Que, Yuqiong ; Wang, Yingbin ; Xu, Longfa ; Chang, Sijia ; Deng, Weixi ; Li, Yue ; Zhu, Rui ; Xu, Jiaxin ; Yang, Hongwei ; Wu, Yuanyuan

Rhinovirus C (RV-C) is the primary causative agent of severe acute respiratory illnesses (ARTIs) in infants and young children. The limited availability of animal models complicates the development of prophylactic and therapeutic strategies targeting RV-C. Previous studies have identified human cadherin-related family member 3 (hCDHR3) as the cellular receptor for RV-C, with its expression enabling previously unsusceptible cells to support both viral entry and replication. Recently, an adult hCDHR3 transgenic mouse model was developed to investigate the role of human stimulator of interferon genes (hSTING) in RV-C15 infection in vivo. However, adult mice do not support efficient RV-C15 infection. Here, we report a transgenic mouse line expressing hCDHR3 constitutively that is highly susceptible to early-life infections by multiple serotypes of RV-C, including RV-C15, RV-C2, and RV-C41. Neonatal transgenic mice infected with various RV-C strains via the intraperitoneal (i.p.) route exhibit similar symptoms, such as severe inflammation, limb paralysis, and death. Moreover, passive immunization with antisera or therapeutic antibodies can protect against lethal RV-C infection in these transgenic mice. Overall, this study provides a valuable animal model for the in vivo antiviral evaluation against RV-C.

01 Feb 2025·Placenta

Profiling epithelial viral receptor expression in amniotic membrane and nasal epithelial cells at birth

Article

Author: Renouf, Bailee ; Berry, Luke ; Lim, James ; Sutanto, Erika N ; Stick, Stephen M ; D'Vaz, Nina ; Amin, Minda ; Kicic-Starcevich, Elizabeth ; Hoyne, Gerard F ; Kidd, Courtney ; Iosifidis, Thomas

INTRODUCTIONChildren with wheeze and asthma present with airway epithelial vulnerabilities, such as impaired responses to viral infection. It is postulated that the in utero environment may contribute to the development of airway epithelial vulnerabilities. The aims of the study were to establish whether the receptors for rhinovirus (RV), respiratory syncytial virus (RSV) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are expressed in the amniotic membrane and whether the pattern of expression is similar to newborn nasal epithelium.METHODSPlacenta were collected (n = 33) from newborns in AERIAL, a sub-study nested under the ORIGINS birth cohort. Using purified RNA from amniotic samples (n = 33), along with previously extracted RNA from nasal epithelial cells from newborns (n = 20), real-time quantitative polymerase chain reaction (qPCR) was performed to determine gene expression of viral receptors for RV, RSV and SARS-CoV-2 in both amniotic and newborn nasal epithelial samples. In addition, receptor protein expression was quantified through Western blot and localised using immunohistochemical staining in amniotic samples.RESULTSAmniotic and newborn nasal samples expressed various receptors for RV (ICAM-1, LDLR, CDHR3), RSV (NCL, CX3CR1) and SARS-CoV-2 (ACE2, TMPRSS2) at the gene level, although the magnitude of expression varied. In addition, protein expression of these receptors was confirmed in the amniotic samples. These proteins were localised to the epithelial layer of the amniotic membrane.CONCLUSIONThis proof-of-concept study indicates the potential of amniotic samples to facilitate investigation into the interactions between the in utero environment and prenatal programming of epithelial innate immune responses to viruses.

01 Feb 2025·Journal of Allergy and Clinical Immunology

The rs6967330 minor allele in CDHR3 is a significant risk factor for severe acute exacerbations in chronic rhinosinusitis

Article

Author: Stern, Debra A ; Le, Christopher H. ; Starks, Rebekah ; Irish, Joseph ; Martinez, Fernando D ; Stern, Debra A. ; Volpe, Sophia ; Palumbo, Sunny ; Martinez, Fernando D. ; Narendran, Nirushan ; Chang, Eugene H ; Chang, Eugene H. ; Bosco, Anthony ; Le, Christopher H

BACKGROUNDAcute exacerbations of chronic rhinosinusitis (AECRS) are commonly triggered by rhinovirus (RV) infections with secondary bacterial infections. Risk factors for AECRS are not well understood.OBJECTIVEWe sought to determine whether carriers of the minor allele rs6967330 (AA/AG) in the cadherin-related family member 3 (CDHR3) gene have an increased risk for RV infections in AECRS in vivo and identify CDHR3 genotype-dependent host responses to RV infection in differentiated nasal airway-liquid interface (ALI) cultures ex vivo.METHODSWe performed a prospective year-long study of adult subjects with chronic rhinosinusitis by the rs6967330 genotype (AA/AG, n = 16; GG, n = 38). We contacted subjects every 2 weeks, and if they reported AECRS, then clinical data were collected. ALI cultures of adults with chronic rhinosinusitis (AG/AA, n = 19; GG, n = 19) were challenged with RV-A and RV-C. We measured viral copy numbers at 4 and 48 hours postinfection and RNA transcriptomes and cytokines at 48 hours postinfection.RESULTSSubjects with the minor allele had significantly higher rates of RV and bacterial infections than those with the major allele. ALI minor allele cultures had higher viral copy numbers of RV-A and RV-C after 48 hours compared with the major allele. Differentially expressed genes and pathways identified an upregulation of IL-10 and IL-4/IL-13 pathways and a significant downregulation of Toll-like receptor pathways in the minor allele cultures after RV-A and RV-C infection. Unsupervised hierarchical analysis of all differentially expressed genes suggested that allergic rhinitis had an additive effect on this response.CONCLUSIONSThe rs6967330 minor allele is associated with increased RV-A and RV-C replication, downregulation of Toll-like receptor-mediated responses, and increased type-2 and cytokine and chemokine responses during RV infection.

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