Target intelligence / Profile preview

Interleukin-10 receptor subunit alpha (IL10RA)

Target
IL10RA
Molecular classification
Receptor, Type II cytokine receptor, Membrane protein, IL-10 receptor family
01

Overview

Interleukin-10 receptor subunit alpha is a membrane-bound protein receptor that serves as the ligand-binding site for the anti-inflammatory cytokine interleukin-10 (IL-10). It is structurally related to interferon receptors and forms a heterotetrameric complex with the β subunit (IL10RB); this complex is primarily expressed on hematopoietic cells. Upon binding IL-10, the alpha subunit undergoes conformational changes that enable signal transduction through associated kinases JAK1 and TYK2, which phosphorylate STAT3, driving transcriptional changes that suppress proinflammatory cytokine synthesis and promote immune regulation. Genetic mutations in IL10RA have been linked to immunological disorders, notably early-onset inflammatory bowel syndromes and immune deficiencies. The receptor is a key modulator of mucosal and systemic immune responses and is considered a candidate for therapeutic intervention in autoimmune, inflammatory, and infectious diseases[1][2][3][7][8].

Other names
CDw210aCD210Interleukin-10 αInterleukin 10 receptor, alphaIL-10RA
02

Mechanism of action

Agonists: Enhance IL-10-mediated anti-inflammatory signaling, leading to inhibition of proinflammatory cytokine production and immune cell modulation (JAK1/TYK2/STAT3 pathway activation). Hypothetical antagonists: Would block IL-10 signaling, potentially increasing inflammation.

03

Biological functions

Immune response modulationSignal transductionAnti-inflammatory actionInhibition of proinflammatory cytokine synthesisPromotion of survival in myeloid progenitor cellsRegulation of gene transcription via JAK/STAT pathway
04

Disease associations

Inflammation (especially in mucosal and gastrointestinal diseases)Infection (host defense modulation)Autoimmune disordersCancer (role in immune evasion and tumor microenvironment)Irritable bowel disease (mutations linked to early onset)
05

Safety considerations

Immunosuppression resulting from agonism may increase risk for infections and tumor progression.Loss-of-function mutations increase the risk of severe, early-onset inflammatory bowel disease.Therapeutic targeting may alter host resistance to pathogens or tumor surveillance
06

Interacting drugs

There are currently no direct drugs or pharmacological agents approved that specifically target IL10RA as antagonists or agonists in clinical practice. However, biologics such as recombinant interleukin-10 protein are used experimentally; the receptor is a potential drug target but not currently known to have approved interacting drugs

1 more in the full profile.

07

Biomarkers

Mutations or expression levels of IL10RA or its downstream signaling components (JAK1, TYK2, STAT3) may serve as biomarkers in inflammatory bowel disease, immune deficiency, and autoimmune disorders

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