Last update 01 Nov 2024

IFNLR1

Last update 01 Nov 2024

Basic Info

Synonyms

CRF2-12, CRF2/12, Cytokine receptor class-II member 12

+ [17]

Introduction

The IFNLR1/IL10RB dimer is a receptor for the cytokine ligands IFNL2 and IFNL3 and mediates their antiviral activity. The ligand/receptor complex stimulate the activation of the JAK/STAT signaling pathway leading to the expression of IFN-stimulated genes (ISG), which contribute to the antiviral state. Determines the cell type specificity of the lambda interferon action. Shows a more restricted pattern of expression in the epithelial tissues thereby limiting responses to lambda interferons primarily to epithelial cells of the respiratory, gastrointestinal, and reproductive tracts. Seems not to be essential for early virus-activated host defense in vaginal infection, but plays an important role in Toll-like receptor (TLR)-induced antiviral defense. Plays a significant role in the antiviral immune defense in the intestinal epithelium.

Drugs associated with IFNLR1

Peginterferon lambda-1a(ZymoGenetics, Inc.)

Target

IFNLR1

Mechanism

IFNLR1 agonists

Active Org.

Eiger BioPharmaceuticals, Inc.

Originator Org.

ZymoGenetics, Inc.

Active Indication

COVID-19 [+1]

Inactive Indication

Chronic hepatitis C genotype 1 [+7]

Drug Highest PhasePhase 3

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

rSIFN-co

Target

IFNLR1

Mechanism

IFNLR1 agonists

Active Org.

Sichuan Huiyang Life-Engineering Co. Ltd.

Originator Org.

Sichuan Huiyang Life-Engineering Co. Ltd.

Active Indication

Hepatitis B, Chronic [+1]

Inactive Indication

Advanced Malignant Solid Neoplasm [+5]

Drug Highest PhasePhase 3

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

PSP-001

Target

IFNLR1

Mechanism

IFNLR1 agonists

Active Org.

Prosit Sole Biotechnology

Originator Org.-

Active Indication

Norovirus Infections

Inactive Indication

Hepatitis B

Drug Highest PhaseIND Application

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Clinical Trials associated with IFNLR1

CTRI/2024/10/074574 / Not yet recruitingPhase 2/3IIT

Topical interferon as a newer treatment modality for uveitic and pseudophakic macular edema:A tertiary care centre study of northern india - NIL

Start Date11 Oct 2024

Sponsor / Collaborator-

ISRCTN10449048 / RecruitingPhase 2IIT

Can interferon gamma prevent infection in critically ill patients at highest risk? A phase II randomised controlled trial - INFINIT (INterFeron to reduce INfection in InTensive care units)

Start Date29 Apr 2024

Sponsor / Collaborator

The Newcastle upon Tyne Hospitals NHS Foundation Trust

ChiCTR2400082602 / SuspendedPhase 4IIT

A real-world study of long-acting interferon guided by ?HBsAg levels in the treatment of HBeAg-negative patients with chronic HBV infection

Start Date01 Apr 2024

Sponsor / Collaborator-

100 Clinical Results associated with IFNLR1

100 Translational Medicine associated with IFNLR1

0 Patents (Medical) associated with IFNLR1

181

Literatures (Medical) associated with IFNLR1

01 Nov 2024·Developmental & Comparative Immunology

Molecular characteristics of rhesus macaque interferon-lambda receptor 1 (mmuIFNLR1): Sequence identity, distribution and alteration after simian-human immunodeficiency virus infection in the skin and buccal mucosa

Article

Author: Liu, Rui-Jie ; Yang, Gui-Bo

Interferon-lambda receptor 1 (IFNLR1) is the key to interferon-lambda's biological activities. Rhesus macaques (Macaca mulatta) are supposedly more suitable for translational studies on interferon lambda-associated human diseases, yet little is known about their IFNLR1 (mmuIFNLR1). In this study, we cloned the coding sequence of mmuIFNLR1, examined its variants, and determined the distribution of mmuIFNLR1 mRNA and immunoreactivity in the buccal mucosa and arm skin of normal and immunodeficiency virus (SHIV/SIV) infected rhesus macaques. It was found that mmuIFNLR1 has 93.1% amino acid sequence identity to that of humans; all the amino acid residues of mmuIFNLR1 signal peptide, transmembrane region, PxxLxF motif and those essential for ligand binding are identical to that of humans; 6 variants of mmuIFNLR1, including the ones corresponding to that of humans were detected; IFNLR1 immunoreactivity was localized in primarily the epithelia of buccal mucosa and arm skin; SHIV/SIV infection could affect the levels of mmuIFNLR1 mRNA and immunoreactivity. These data expanded our knowledge on mmuIFNLR1 and provided a scientific basis for rational use of rhesus macaques in studies of IFN-λ associated human diseases like AIDS. Future studies testing IFNLR1-targeting therapeutics in rhesus macaques were warranted.

01 Oct 2024·Physiological Reports

Context‐specific anti‐inflammatory roles of type III interferon signaling in the lung in nonviral injuries

Article

Author: Bain, William G. ; Jie, Zhijun ; Kotenko, Sergei V. ; Robinson, Keven M. ; Wang, Victoria D. ; Feng, Jingjing ; Kim, Jooyoung ; Liu, Hongbo ; Chang, De ; Sharma, Lokesh ; Dela Cruz, Charles S.

AbstractType III interferons (λ1, λ2, and λ3) are potent antiviral cytokines in the lung. However, their roles in nonviral lung injuries are less well understood. This study investigates the activation of type III interferon signaling in three distinct models of lung injuries caused by diverse stimuli: the bacterial pathogen Pseudomonas aeruginosa, bacterial endotoxin LPS, and the chemotherapeutic agent bleomycin. Our data show that, despite inducing a potent inflammatory response, Pseudomonas and LPS did not increase IFNλ secretion. In contrast, bleomycin instillation increased secretion of IFNλ in the airways at both early and late time points. Consistent with limited secretion, type III interferon signaling had a minimal role in the host response to both Pseudomonas and LPS, as measured by pathogen burden, inflammatory response, and lung injury. Conversely, a deficiency in type III interferon signaling led to increased inflammatory signaling and elevated acute lung injury in the bleomycin model on day 3. This elevated early injury resulted in impaired recovery in IFNLR1 knockout mice, as evidenced by their recovery from bleomycin‐induced weight loss. Taken together, these data suggest a context‐specific activation of type III interferon signaling, where it plays an anti‐inflammatory role in the lung.

17 Jul 2024·mBio

Type III interferon drives pathogenicity to Staphylococcus aureus via the airway epithelium

Article

Author: Parker, Dane ; Kaiser, Katherine ; Pires, Silvia

ABSTRACT Type III interferon signaling contributes to the pathogenesis of the important human pathogen Staphylococcus aureus in the airway. Little is known of the cellular factors important in this response. Using Ifnl2 -green fluorescent protein reporter mice combined with flow cytometry and cellular depletion strategies, we demonstrate that the alveolar macrophage is the primary producer of interferon lambda (IFN-λ) in response to S. aureus in the airway. Bone marrow chimeras showed reduced bacterial burden in IFN-λ receptor (IFNLR1)-deficient recipient mice, indicative that non-hematopoietic cells were important for pathogenesis, in addition to significant reductions in pulmonary inflammation. These observations were confirmed through the use of an airway epithelial-specific IFNLR knockout mouse. Our data suggest that upon entry to the airway, S. aureus activates alveolar macrophages to produce type III IFN that is subsequently sensed by the airway epithelium. Future steps will determine how signaling from the epithelium then exerts its influence on bacterial clearance. These results highlight the important, yet sometimes detrimental, role of type III IFN signaling during infection and the impact the airway epithelium plays during host–pathogen interactions. IMPORTANCE The contribution of type III interferon signaling to the control of bacterial infections is largely unknown. We have previously demonstrated that it contributes to the pathogenesis of acute Staphylococcus aureus respiratory infection. In this report, we document the importance of two cell types that underpin this pathogenesis. We demonstrate that the alveolar macrophage is the cell that is responsible for the production of type III interferon and that this molecule is sensed by airway epithelial cells, which impacts both bacterial clearance and induction of inflammation. This work sheds light on the first two aspects of this important pathogenic cascade.

News (Medical) associated with IFNLR1

16 Mar 2022

·www.biospace.com

Eiger BioPharmaceuticals to Host Conference Call to Discuss Phase 3 TOGETHER Study Results of Peginterferon Lambda for COVID-19 on Thursday, March 17, 2022

Eiger BioPharmaceuticals, Inc (Nasdaq:EIGR), a commercial-stage biopharmaceutical company focused on the development of innovative therapies to treat and cure Hepatitis Delta Virus (HDV) and other serious diseases, today announced that it will host a conference call on Thursday, March 17, 2022, at 5:30 AM Pacific / 8:30 AM Eastern, to discuss the results from the Phase 3 TOGETHER study of Peginterferon Lambda for COVID-19. The live and replayed webcast of the call will be available through the company's website at . To participate in the live call by phone, dial (844) 743-2495 (U.S.) or (661) 378-9529 (International) and enter conference ID 8990285. The webcast will be archived and available for replay for at least 90 days after the event.

COVID-19Peginterferon lambda-1a(ZymoGenetics, Inc.)

26 May 2021

·www.biospace.com

Prosit Sole Biotechnology Initiates First-In-Human Clinical Trial of Novel Interferon Lambda Chimera in US

BALTIMORE, May 26, 2021 /PRNewswire/ -- Prosit Sole Biotechnology, a clinical-stage biotech company developing novel protein therapeutics, today announces that it has initiated the first-in-human ("FIH") Phase I clinical trial of PSP001 in US. PSP001 is a novel, long acting and potent interferon lambda chimera injection. The first dose was administered on May 25, 2021. Type III interferons (IFN's), also termed interferon lambda's (IFNλ's) constitute a new addition to the IFN family. Their unique receptor IFNλR1 is particularly abundant at the barrier surfaces, such as the respiratory tracts, the gastrointestinal tracts, and the liver. Non-redundant to type I interferons (IFNα and IFNβ), IFNλ's exhibit unique antiviral and immune modulatory activities. Prosit Sole Biotechnology is developing PSP001 for the treatment of chronic norovirus enteritis in hematopoietic and solid organ transplant recipients. "Chronic norovirus enteritis in immunocompromised patients is an urgent unmet medical need. There are no approved therapies for this debilitating disease." said Hongyu Liu, PhD, CEO of Prosit Sole Biotechnology. "We are also actively developing PSP001 for additional indications such as chronic hepatitis B." Investor Contact: Email: liuhongyu@prositsole.com Cindy Yu Email: cindy.yu@prositsole.com 010-62975234 Source: Prosit Sole Biotechnology To learn more, please visit View original content: SOURCE Prosit Sole Biotechnology (Beijing) Co., Ltd.

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IFNLR1

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