Target intelligence / Profile preview

Interleukin-10 receptor subunit beta (IL10RB) (IL10RB)

Target
IL10RB
Molecular classification
Receptor, Cytokine receptor, Class II cytokine receptor family
01

Overview

Interleukin-10 receptor subunit beta (IL10RB) is a type II cytokine receptor that serves as a common accessory subunit for several signaling complexes within the IL-10 family. Unlike the ligand-specific alpha subunits, IL10RB is ubiquitously expressed across various tissues and is essential for the functional assembly of receptors for IL-10, IL-22, IL-26, and type III interferons (IFN-lambda). Upon ligand binding to the primary receptor subunit, IL10RB is recruited to the complex, where it facilitates the activation of Janus kinase 2 (JAK2) or Tyrosine kinase 2 (Tyk2), leading to the phosphorylation of Signal Transducer and Activator of Transcription 3 (STAT3). This signaling pathway is a master regulator of anti-inflammatory responses, particularly in the gastrointestinal tract, where it maintains mucosal homeostasis. Loss-of-function mutations in the IL10RB gene are strongly associated with very early-onset inflammatory bowel disease (VEO-IBD), a severe condition characterized by intractable intestinal inflammation. Therapeutic strategies involving IL10RB focus on the use of recombinant cytokines or fusion proteins, such as pegilodecakin and efmarodocokin alfa, to treat chronic inflammatory diseases, promote tissue regeneration, or provide antiviral defense. However, because IL10RB is a shared component of multiple cytokine pathways, pharmacological modulation requires careful consideration of potential off-target effects and systemic immunosuppression.

Other names
Interleukin-10 receptor 2IL-10R2IL-10RBCytokine receptor family 2 member 4CRFB4CDw210bCRF2-4D21S58
02

Mechanism of action

Agonism of the receptor complex to activate JAK/STAT signaling (primarily STAT3) for anti-inflammatory or tissue-protective effects

03

Biological functions

Signal transductionImmune responseAnti-inflammatory responseAntiviral defenseTissue repairCytokine signaling
04

Disease associations

Inflammatory bowel diseaseInflammationInfectionCancerAutoimmune diseaseVery early-onset inflammatory bowel disease (VEO-IBD)
05

Safety considerations

ImmunosuppressionIncreased risk of infectionOff-target effects due to shared subunit usage across multiple cytokine pathwaysPotential for cytokine release syndromeEngraftment failure in hematopoietic stem cell transplantation
06

Interacting drugs

Pegilodecakin

4 more in the full profile.

07

Biomarkers

STAT3 phosphorylation (pSTAT3)IL10RB gene mutationsInterleukin-10 (IL-10) levelsInterleukin-6 (IL-6) levelsStool occult blood

Beyond the preview

Go deeper on Interleukin-10 receptor subunit beta (IL10RB) (IL10RB).

Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.

Drug pipeline

Full profile access

Explore the programs pursuing this target and their development progress.

  • Drug candidates
  • Developers
  • Development stage

Clinical trials

Full profile access

Follow the clinical studies evaluating therapies directed at this target.

  • Trial design
  • Status
  • Readouts

Competitive landscape

Full profile access

Compare approaches across drug candidates, modalities, and indications.

  • Programs
  • Modalities
  • Indications

Literature & evidence

Full profile access

Investigate the research and source evidence behind target biology and development.

  • Publications
  • Sources
  • Analysis

Patents

Full profile access

Explore patent activity around therapies and technologies addressing this target.

  • Patents
  • Assignees
  • Technologies

Research & analysis

Full profile access

Connect target biology, drug development, and emerging evidence in your research.

  • Biology
  • Development news
  • Analysis

Bring the full picture into focus.

See how Gosset can support your research on Interleukin-10 receptor subunit beta (IL10RB) (IL10RB).

Explore the full profile

Gosset Free

Get started with Gosset.

Enter your work email and we’ll be in touch with next steps.

Work email preferred.

Book a call