Protein / target

Interleukin-10

Encoded byIL10P22301Homo sapiensSwiss-Prot

UniProt: P22301 Ensembl: ENSG00000136634 HGNC: HGNC:5962 NCBI Gene: 3586

Clinical-stage

Therapeutic maturity

Clinical candidates

Small-molecule tractable

Druggability

Med-Quality Pocket

Research papers

Protein at a glance

Biological role

Interleukin-10 receptor binding

Strongest disease association

Colitis, Ulcerative

Via encoding gene IL10 · Genetic evidence · score 0.88

Therapeutic position

Clinically advancing target

Antibodies

Research activity

Emerging research

19 papers · latest 2024

Derived from structured UniProt, Open Targets and literature data on this page.

Protein profile

UniProt 2026_02

Canonical identity and biological annotation from UniProt.

Function overview

Major immune regulatory cytokine that acts on many cells of the immune system where it has profound anti-inflammatory functions, limiting excessive tissue disruption caused by inflammation.

View complete UniProt function annotation

Major immune regulatory cytokine that acts on many cells of the immune system where it has profound anti-inflammatory functions, limiting excessive tissue disruption caused by inflammation. Mechanistically, IL10 binds to its heterotetrameric receptor comprising IL10RA and IL10RB leading to JAK1 and STAT2-mediated phosphorylation of STAT3 (PubMed:16982608). In turn, STAT3 translocates to the nucleus where it drives expression of anti-inflammatory mediators (PubMed:18025162). Targets antigen-presenting cells (APCs) such as macrophages and monocytes and inhibits their release of pro-inflammatory cytokines including granulocyte-macrophage colony-stimulating factor /GM-CSF, granulocyte colony-stimulating factor/G-CSF, IL-1 alpha, IL-1 beta, IL-6, IL-8 and TNF (PubMed:11564774, PubMed:1940799, PubMed:7512027). Also interferes with antigen presentation by reducing the expression of MHC-class II and co-stimulatory molecules, thereby inhibiting their ability to induce T cell activation (PubMed:8144879). In addition, controls the inflammatory response of macrophages by reprogramming essential metabolic pathways including mTOR signaling (By similarity)

Subcellular location

Secreted

Domains and Gene Ontology detail (72)

Gene Ontology

Cextracellular region
Cextracellular space
Fcytokine activity
Fgrowth factor activity
Finterleukin-10 receptor binding
Fprotein dimerization activity
PB cell differentiation
PB cell proliferation
Pcell surface receptor signaling pathway via JAK-STAT
Pcellular response to estradiol stimulus
Pcellular response to lipopolysaccharide
Pcytokine-mediated signaling pathway

178 aa · 21 kDa

Biological roles

What this protein does, drawn together from its UniProt function, Gene Ontology terms and Reactome pathways.

Cell proliferation & survivalGOSynaptic signallingGOCell migrationGOCell-cycle regulationGOImmune signallingUniProt · GOTranscriptional regulationGO

View supporting evidence

Cell proliferation & survival

·negative regulation of cell population proliferation
·positive regulation of cell population proliferation

Synaptic signalling

·regulation of synapse organization

Cell migration

·leukocyte chemotaxis

Cell-cycle regulation

·negative regulation of mitotic cell cycle

Immune signalling

·Major immune regulatory cytokine that acts on many cells of the immune system where it h…
·cytokine activity
·interleukin-10 receptor binding
·B cell differentiation

Transcriptional regulation

·positive regulation of DNA-templated transcription
·positive regulation of miRNA transcription
·positive regulation of transcription by RNA polymerase II
·regulation of gene expression

Concepts derived from UniProt GO Reactome — each badge above shows which sources supported that role.

Translational evidence

Open Targets 26

Why this target matters therapeutically, strongest evidence first. Disease associations are gene-level (via the gene that encodes this protein) and open into the full confidence synthesis; the development universe, tractability and safety annotations are target-level, from Open Targets.

Strongest disease associations · via encoding gene IL10

Gene-level evidence surfaced through the gene IL10that encodes this protein — not a direct protein–disease relationship. Ranked by Forefront's causal-directness weighting, so genetically- and clinically-evidenced diseases lead over ones that merely share the literature.

Colitis, Ulcerative

0.89Well supported

Genetic evidence dominant · Open Targets 0.55

Lupus Erythematosus, Systemic

0.86Well supported

Genetic evidence dominant · Open Targets 0.52

Diabetes Mellitus, Type 1

0.85Well supported

Genetic evidence dominant · Open Targets 0.53

Crohn's Disease

0.85Well supported

Genetic evidence dominant · Open Targets 0.61

Inflammatory Bowel Diseases

0.80Well supported

Genetic evidence dominant · Open Targets 0.59

View evidence synthesis (5)

Colitis, UlcerativeWell supported

0.89

agreement 0.76–1.00

Genetic94%Literature6%RNA expression1%

Open Targets aggregate 0.55 · 3 independent evidence families

Lupus Erythematosus, SystemicWell supported

0.86

agreement 0.75–0.97

Genetic73%Literature13%Animal model13%RNA expression1%

Open Targets aggregate 0.52 · 4 independent evidence families

Diabetes Mellitus, Type 1Well supported

0.85

agreement 0.72–0.99

Genetic87%Literature13%

Open Targets aggregate 0.53 · 2 independent evidence families

Crohn's DiseaseWell supported

0.85

agreement 0.71–0.99

Genetic94%Literature7%Genetic literaturedup

Open Targets aggregate 0.61 · 2 independent evidence families · 1 not counted as duplicate

Inflammatory Bowel DiseasesWell supported

0.80

agreement 0.66–0.94

Genetic84%Literature16%

Open Targets aggregate 0.59 · 2 independent evidence families

This ranking differs from Open Targets' own: re-weighting moves genetically-evidenced diseases above more heavily co-mentioned ones. The evidence agreement range shows how closely the independent evidence families agree — it is not a statistical confidence interval, and nothing here is fitted to outcome data. Derived from Open Targets evidence types under Forefront weighting; the per-type scores above show the calculation.

Show all associations

Crohn's Disease0.61

Inflammatory Bowel Diseases0.59

Colitis, Ulcerative0.55

Diabetes Mellitus, Type 10.53

Lupus Erythematosus, Systemic0.52

Arthritis, Rheumatoid0.48

Behcet's Syndrome0.43

Ulcer0.43

Drug development

1 compounds recorded · 1 in clinical development

Open Targets' development universe — every compound recorded against the target at any stage, not all approved medicines.

View all recorded compounds (1)

SCH-708980Phase 1 2

Open Targets known-drugs universe. Drug name and highest clinical stage only — the disease relationship is NOT read from this slice (it carries trial-context noise); approved indications come from the canonical graph above.

Tractability

Small molecules — Emerging

Feasibility evidence (med-quality pocket) — no clinical-stage drug of this modality recorded.

Antibodies — Strong

Advanced Clinical and GO CC high conf support this modality.

View underlying tractability evidence (5)

SM · Med-Quality PocketAB · Advanced ClinicalAB · GO CC high confAB · UniProt loc med confAB · UniProt SigP or TMHMM

Raw Open Targets tractability assessment buckets, by modality.

Safety-related annotations

a hypersensitivity reaction to NSAIDsClinPGxhypersensitivity reaction to NSAIDsClinPGxDrug HypersensitivityClinPGx

Terms indexed against this target in Open Targets' safety data, with their datasource. These are annotations, not causal claims: the direction of effect (whether activation or inhibition is implicated), species and evidence strength are not captured here, so an entry does not mean that modulating this target is known to cause that condition.