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Protein / target

Interleukin-4

Encoded byIL4P05112Homo sapiensSwiss-Prot
Clinical-stage
Therapeutic maturity
2
Clinical candidates
Antibody-tractable
Druggability
Advanced Clinical
13
Research papers

Protein at a glance

Biological role

Interleukin-4 receptor binding

Strongest disease association

Ischemic Stroke

Via encoding gene IL4 · Genetic literature evidence · score 0.61

Therapeutic position

Clinically advancing target

Antibodies

Research activity

Emerging research

13 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

Cytokine secreted primarily by mast cells, T-cells, eosinophils, and basophils that plays a role in regulating antibody production, hematopoiesis and inflammation, and the development of effector T-cell responses.

View complete UniProt function annotation

Cytokine secreted primarily by mast cells, T-cells, eosinophils, and basophils that plays a role in regulating antibody production, hematopoiesis and inflammation, and the development of effector T-cell responses (PubMed:1993171, PubMed:3016727). Induces the expression of class II MHC molecules on resting B-cells. Enhances both secretion and cell surface expression of IgE and IgG1 (PubMed:1993171). Also regulates the expression of the low affinity Fc receptor for IgE (CD23) on both lymphocytes and monocytes (PubMed:2521231). Positively regulates IL31RA expression in macrophages. Stimulates autophagy in dendritic cells by interfering with mTORC1 signaling and through the induction of RUFY4. In addition, plays a critical role in higher functions of the normal brain, such as memory and learning (By similarity). Upon binding to IL4, IL4R receptor dimerizes either with the common IL2R gamma chain/IL2RG to produce the type 1 signaling complex, located mainly on hematopoietic cells, or with the IL13RA1 to produce the type 2 complex, which is also expressed on nonhematopoietic cells (PubMed:10219247, PubMed:11526337, PubMed:18243101). Engagement of both types of receptors initiates JAK3 and to a lower extend JAK1 phosphorylation leading to activation of the signal transducer and activator of transcription 6/STAT6 (PubMed:7721895)

Subcellular location

Secreted
Domains and Gene Ontology detail (51)

Gene Ontology

  • Cextracellular region
  • Cextracellular space
  • Fcytokine activity
  • Fgrowth factor activity
  • Finterleukin-4 receptor binding
  • PB cell differentiation
  • Pcell surface receptor signaling pathway via JAK-STAT
  • Pcholesterol metabolic process
  • Pdendritic cell differentiation
  • Pimmune response
  • Pinterleukin-4-mediated signaling pathway
  • Pmacrophage activation

153 aa · 17 kDa · 2 isoforms

Biological roles

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

Cell migrationGOCell proliferation & survivalGOLipid & lipoprotein metabolismGOImmune signallingUniProt · GOTranscriptional regulationUniProt · GOApoptosis & cell deathGO
View supporting evidence

Cell migration

  • ·negative regulation of epithelial cell migration
  • ·positive regulation of cell migration

Cell proliferation & survival

  • ·positive regulation of cell population proliferation

Lipid & lipoprotein metabolism

  • ·cholesterol metabolic process

Immune signalling

  • ·Cytokine secreted primarily by mast cells, T-cells, eosinophils, and basophils that play…
  • ·cytokine activity
  • ·interleukin-4 receptor binding
  • ·B cell differentiation

Transcriptional regulation

  • ·Cytokine secreted primarily by mast cells, T-cells, eosinophils, and basophils that play…
  • ·negative regulation of DNA-templated transcription
  • ·negative regulation of transcription by RNA polymerase II
  • ·positive regulation of DNA-templated transcription

Apoptosis & cell death

  • ·negative regulation of apoptotic process
  • ·negative regulation of endothelial cell apoptotic process

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 IL4

Gene-level evidence surfaced through the gene IL4that 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.

Asthma
0.54Moderately supported

Genetic evidence dominant · Open Targets 0.28

Ischemic Stroke
0.50Moderately supported

Genetic literature evidence dominant · Open Targets 0.38

Dermatitis, Atopic
0.46Limited support

Genetic evidence dominant · Open Targets 0.27

Dermatitis, Seborrheic
0.43Limited support

Genetic evidence dominant · Open Targets 0.26

Erythematosquamous dermatosis
0.40Limited support

Genetic evidence dominant · Open Targets 0.24

View evidence synthesis (5)
AsthmaModerately supported
0.54
agreement 0.440.65
Genetic60%Literature22%Clinical17%

Open Targets aggregate 0.28 · 3 independent evidence families

Ischemic StrokeModerately supported
0.50
agreement 0.350.66
Genetic literature93%Literature7%

Open Targets aggregate 0.38 · 2 independent evidence families

Dermatitis, AtopicLimited support
0.46
agreement 0.320.60
Genetic86%Literature14%

Open Targets aggregate 0.27 · 2 independent evidence families

Dermatitis, SeborrheicLimited support
0.43
agreement 0.290.57
Genetic99%Literature1%

Open Targets aggregate 0.26 · 2 independent evidence families

Erythematosquamous dermatosisLimited support
0.40
agreement 0.280.52
Genetic100%

Open Targets aggregate 0.24 · 1 independent evidence family

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
Ischemic Stroke0.38
Asthma0.28
Dermatitis, Atopic0.27
Dermatitis, Seborrheic0.26
Erythematosquamous dermatosis0.24
Hypersensitivity0.22
Respiratory Tract Diseases0.20
Rhinitis, Allergic0.20
Psoriasis0.19
Childhood onset asthma0.18

Drug development

2 compounds recorded · 2 in clinical development

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

View all recorded compounds (2)
PASCOLIZUMABPhase 2
ROMILKIMABPhase 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

AntibodiesStrong

Advanced Clinical and GO CC high conf support this modality.

View underlying tractability evidence (4)
AB · 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

aspirin-induced decline in forced expiratory volume in 1 s (FEV1)ClinPGx

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.

Research activity

13 papers · to 2024

Papers linked directly to this protein. This is the protein's own literature — descriptor-derived papers are kept separate below.

Most cited

Orihuela R · British journal of pharmacology · 2016

Romani N · The Journal of experimental medicine · 1994

Sallusto F · The Journal of experimental medicine · 1998

Recent

Microglial M1/M2 polarization and metabolic states.

Orihuela R · British journal of pharmacology · 2016

The IL-23/IL-17 axis in inflammation.

Iwakura Y · The Journal of clinical investigation · 2006

Europe PMC papers linked directly to this protein.