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Last update 08 May 2025

IFNAR x IFNβ

Last update 08 May 2025

Basic Info

Related Targets

IFNARIFNβ

Drugs associated with IFNAR x IFNβ

ART-I02

Target

IFNAR x IFNβ

Mechanism

IFNAR agonists [+1]

Active Org.

Academic Medical Center University of Amsterdam [+1]

Originator Org.

MeiraGTx Netherlands BV

Active Indication

Rheumatoid Arthritis

Inactive Indication

Osteoarthritis

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with IFNAR x IFNβ

NCT03445715

/ Unknown statusPhase 1

A Single Dose Clinical Trial to Study the Safety of ART-I02 in Patients With Rheumatoid Arthritis

Start Date03 Jan 2018

Sponsor / Collaborator

MeiraGTx Netherlands BV

NCT02727764

/ Unknown statusPhase 1

A Single Dose Clinical Trial to Study the Safety of ART-I02 in Patients With Arthritis

This study will evaluate the safety and tolerability of a single intra-articular administration of ART-I02 (AAV5.NF-kB.IFN-β), a recombinant adeno-associated virus (AAV) type 2/5 vector in subjects with Rheumatoid Arthritis (RA) or Osteoarthritis (OA) and active arthritis of the carpometacarpal (CMC), metacarpophalangeal (MCP), proximal interphalangeal (PIP), or distal interphalangeal (DIP) joints.

Start Date20 Apr 2017

Sponsor / Collaborator

MeiraGTx Netherlands BV

[+1]

100 Clinical Results associated with IFNAR x IFNβ

100 Translational Medicine associated with IFNAR x IFNβ

0 Patents (Medical) associated with IFNAR x IFNβ

552

Literatures (Medical) associated with IFNAR x IFNβ

01 Jun 2025·Life Sciences

Type I interferon protects against bone loss in periodontitis by mitigating an interleukin (IL)-17-neutrophil axis

Article

Author: Marchesan, Julie T ; Lin, Maoxuan ; Zhang, Jinmei ; Williamson, Megumi A ; Moss, Kevin ; Sun, Hongli ; Zeng, Erliang ; Lei, Yu Leo ; Miao, Di ; Ding, Qiong ; Shi, Wei ; Zhang, Shaoping ; Yu, Ning ; Wang, Angela X

Type I interferons (IFNs-I), a group of pleiotropic cytokines, critically modulate host response in various inflammatory diseases. However, the role of the IFN-I pathway in periodontitis remains largely unknown. In this report, we describe that the IFN-β levels in the gingival crevicular fluid of human subjects were negatively associated with periodontitis and clinical gingival inflammation. Disruption of IFN-I signaling worsened alveolar bone resorption in a ligature-induced periodontitis murine model. Deficiency of the IFN-I pathway resulted in an exaggerated inflammatory response in myeloid cells and drastically increased the interleukin-17 (IL-17)-mediated neutrophil recruitment in the gingiva. We further identified that the myeloid lineage-specific IFN-I response was essential in safeguarding against periodontal inflammation by suppressing the IL-17-producing γδ T cells in gingiva. IFN-I signaling also directly repressed osteoclastogenesis in monocytes, which are precursor cells for osteoclasts. Therefore, our findings demonstrate that an integral myeloid-specific IFN-I pathway protects against bone loss by keeping the IL-17-neutrophil axis in check and directly inhibiting osteoclast formation in periodontitis.

01 Apr 2025·Immunology Letters

Gut TLRs and IFN pathways mRNA expression and frequencies of CD4+ T cell expressing CD38 or HLA-DR go in parallel during HIV immunopathogenesis

Article

Author: Fracella, Matteo ; Ceccarelli, Giancarlo ; d'Ettorre, Gabriella ; Mastroianni, Claudio M ; Lazzaro, Alessandro ; Frasca, Federica ; Bugani, Ginevra ; Santinelli, Letizia ; Scagnolari, Carolina ; Maddaloni, Luca

While much is known about the expression of interferon (IFN) pathways in the blood of people living with HIV (PLWH), their role in the intesinal tract has only recently been appreciated. The aim of this study was to evaluate gut mRNA expression levels of innate immune genes involved in the HIV-host interaction and their association with CD4⁺T cell immune activation in long-term HAART-experienced PLWH. PLWH had increased intestinal levels of TLR4, type I IFN (IFN-α2, IFN-α14, IFN-β) and IFNAR1 mRNAs, as well as increased frequencies of CD4⁺T lymphocytes expressing CD38 or HLA-DR compared to the healthy donors. Moreover, TLR4, TLR9, IRF3, IRF7 and IFN-α14 mRNA expression was positively correlated with the frequency of CD4⁺T cells expressing CD38 or HLA-DR. These findings suggest a dysregulation of innate immunity, particularly of the TLRs and IFN pathways in the gut of PLWH. Genes in these pathways also appear to correlate with the levels of CD4⁺T cell immune activation.

03 Feb 2025·Journal of Experimental Medicine

A common form of dominant human IFNAR1 deficiency impairs IFN-α and -ω but not IFN-β-dependent immunity

Article

Author: Condino-Neto, Antonio ; Quyen, Do ; Tan, Luong Minh ; Perez de Diego, Rebeca ; Moatti, Jean-Paul ; Flores, Carlos ; Oo, Khin Yi ; Mercado-Garcia, Jesus ; Aguilar-Lopez, Raul ; Fellay, Jacques ; Jouanguy, Emmanuelle ; Temel, Sehime Gulsun ; Mansouri, Davood ; Leung, Daniel ; Bunleat, M. ; Lecuit, Marc ; Hung, Tran Thi Mai ; Bun, Kimrong ; Novelli, Giuseppe ; Tangye, Stuart G. ; Singh, Neha ; Devaux, Christian ; Soler-Palacin, Pere ; Pesole, Graziano ; Alcantara-Garduno, Ana Bertha ; Zhang, Qian ; Laurent, Denis ; Casanova, Jean-Laurent ; Bizien, Lucy ; Feldman, Hagit Baris ; Thuy, Nguyen Thi Thu ; Lam, Nguyen Van ; Crabol, Yoann ; Herrant, Magali ; Vongsouvath, Manivanh ; Hafner, Lukas ; Huong, Tran Thi Thu ; Piola, Patrice ; Cobat, Aurelie ; Borghesi, Alessandro ; Perot, Philippe ; Rattanavong, Sayaphet ; Dubot-Peres, Audrey ; July, May ; Vinh, Donald C. ; Tayoun, Ahmad Abou ; Sothy, Heng ; Pham, Anh Tuan ; Sim, M. Kanarith ; Thuy, Phung Bich ; Gorochov, Guy ; Berkun, Yackov ; Honnorat, Jerome ; de Lamballerie, Xavier ; Buchy, Philippe ; Aye, Aye Mya Min ; Colobran, Roger ; Lin, Daniel C. ; Rosset, Bruno ; Bastard, Paul ; Hammoud, Hassan ; Turvey, Stuart E. ; Ozcelik, Tayfun ; Aiuti, Alessandro ; Puel, Anne ; Sharif-Askari, Narjes Saheb ; Rodriguez-Gallego, Carlos ; Bleakley, Kevin ; Trouillet-Assant, Sophie ; Tin, Htay Htay ; Douangnouvong, Anousone ; Tin, Ommar Swe ; Lago, Magali ; Resnick, Igor ; Delfraissy, Jean-Francois ; Brodin, Petter ; Tam, Anthony R. ; Christodoulou, John ; Okada, Satoshi ; Eloit, Marc ; Arias, Andres A. ; Capelle, Julien ; Davong, Viengmon ; Zabaleta-Martinez, Oscar ; Sbeity, Manal ; Hai, Le Thanh ; Murgue, Committee Bernadette ; Renia, Laurent ; Lortholary, Olivier ; Beziat, Vivien ; Phakhounthong, Khansoudaphone ; Lorenzo, Lazaro ; Peres, Auey Dubot ; Ferrant, Catherine ; Keles, Sevgi ; Hung, Ivan Fan-Ngai ; Vongsouvath, Malavanh ; de Prost, Nicolas ; Andreakos, Evangelos ; An, Pham Nhat ; Fakhreddine, Soha ; Le Pen, Jeremie ; Torktaz, Ibrahim ; Milisavljevic, Baptiste ; Moncada-Velez, Marcela ; Sales Luiz Vianna, Fernanda ; Tarantola, Arnaud ; Debre, Patrice ; Novelli, Antonio ; Chommanam, Danoy ; Duval, Xavier ; Jouan, Marc ; Pinto, Anne Laurie ; Hlaing, Chaw Su ; Phuc, Phan Huu ; Materna, Marie ; Mogensen, Trine H. ; Linn, Kyaw ; Franco, Jose Luis ; Kyaw, Latt Latt ; Le-voyer, Tom ; Santy, Ky ; Pedraza-Sanchez, Sigifredo ; de Weerd, Nicole A. ; Meyts, Isabelle ; Bonnet, Pascal ; Chevalier, Veronique ; Bunnakea, Em ; Ozcelik, Firat ; Thorball, Christian ; Anh, Dang Duc ; Sibounheunang, Bountoy ; Huong, Do Thu ; Lau, Yu Lung ; Sedighzadeh, Sahar ; Duong, Veasna ; Dussart, Philippe ; Channa, Mey ; Bolze, Alexandre ; Herrera, Maria Teresa ; Abel, Laurent ; Halwani, Rabih ; Thein, Win ; Gorman, Chris ; Fontenille, Didier ; Seguy, Maud ; Duvlis, Sotirija ; Durand, Benoit ; Oum, MengHeng ; Hertzog, Paul J. ; Hagin, David ; Gregersen, Peter K. ; Zhang, Peng ; Bousfiha, Ahmed A. ; Perez-Tur, Jordi ; Eng, Chanreaksmey ; Uddin, K. M. Furkan ; Panha, M. ; Al Qureshah, Fahd ; El Zein, Loubna ; Seephone, Malee ; Chantratita, Wasun ; Spaan, Andras N. ; Al-Muhsen, Saleh ; Rice, Charles M. ; Shahrooei, Mohammad ; Bhattad, Sagar ; Dundar, Munis ; Tissot-Dupont, Herve ; Hien, Nguyen ; Newton, Paul N. ; Zhang, Shen-Ying ; Thair, Cho ; Vianna, Fernanda ; Mayxay, Mayfong ; Pommier, Jean-David ; Ng, Lisa F. P.

Autosomal recessive deficiency of the IFNAR1 or IFNAR2 chain of the human type I IFN receptor abolishes cellular responses to IFN-α, -β, and -ω, underlies severe viral diseases, and is globally very rare, except for IFNAR1 and IFNAR2 deficiency in Western Polynesia and the Arctic, respectively. We report 11 human IFNAR1 alleles, the products of which impair but do not abolish responses to IFN-α and -ω without affecting responses to IFN-β. Ten of these alleles are rare in all populations studied, but the remaining allele (P335del) is common in Southern China (minor allele frequency ≈2%). Cells heterozygous for these variants display a dominant phenotype in vitro with impaired responses to IFN-α and -ω, but not -β, and viral susceptibility. Negative dominance, rather than haploinsufficiency, accounts for this dominance. Patients heterozygous for these variants are prone to viral diseases, attesting to both the dominance of these variants clinically and the importance of IFN-α and -ω for protective immunity against some viruses.

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