Back to discover

Protein / target

Interleukin-2

Encoded byIL2P60568Homo sapiensSwiss-Prot
Small-molecule tractable
Druggability
Structure with Ligand
22
Research papers

Protein at a glance

Biological role

Kappa-type opioid receptor binding

Strongest disease association

Asthma

Via encoding gene IL2 · Genetic evidence · score 0.77

Research activity

Emerging research

22 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 produced by activated CD4-positive helper T-cells and to a lesser extend activated CD8-positive T-cells and natural killer (NK) cells that plays pivotal roles in the immune response and tolerance.

View complete UniProt function annotation

Cytokine produced by activated CD4-positive helper T-cells and to a lesser extend activated CD8-positive T-cells and natural killer (NK) cells that plays pivotal roles in the immune response and tolerance (PubMed:6438535). Binds to a receptor complex composed of either the high-affinity trimeric IL-2R (IL2RA/CD25, IL2RB/CD122 and IL2RG/CD132) or the low-affinity dimeric IL-2R (IL2RB and IL2RG) (PubMed:16293754, PubMed:16477002). Interaction with the receptor leads to oligomerization and conformation changes in the IL-2R subunits resulting in downstream signaling starting with phosphorylation of JAK1 and JAK3 (PubMed:7973659). In turn, JAK1 and JAK3 phosphorylate the receptor to form a docking site leading to the phosphorylation of several substrates including STAT5 (PubMed:8580378). This process leads to activation of several pathways including STAT, phosphoinositide-3-kinase/PI3K and mitogen-activated protein kinase/MAPK pathways (PubMed:25142963). Functions as a T-cell growth factor and can increase NK-cell cytolytic activity as well (PubMed:6608729). Promotes strong proliferation of activated B-cells and subsequently immunoglobulin production (PubMed:6438535). Plays a pivotal role in regulating the adaptive immune system by controlling the survival and proliferation of regulatory T-cells, which are required for the maintenance of immune tolerance. Moreover, participates in the differentiation and homeostasis of effector T-cell subsets, including Th1, Th2, Th17 as well as memory CD8-positive T-cells

Subcellular location

Secreted
Domains and Gene Ontology detail (39)

Gene Ontology

  • Cextracellular region
  • Cextracellular space
  • Fcarbohydrate binding
  • Fcytokine activity
  • Fglycosphingolipid binding
  • Fgrowth factor activity
  • Finterleukin-2 receptor binding
  • Fkappa-type opioid receptor binding
  • Fkinase activator activity
  • Padaptive immune response
  • Pcell adhesion
  • Pcell surface receptor signaling pathway via JAK-STAT

153 aa · 18 kDa

Biological roles

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

Cell proliferation & survivalGOImmune signallingUniProt · GOApoptosis & cell deathGO
View supporting evidence

Cell proliferation & survival

  • ·positive regulation of cell population proliferation

Immune signalling

  • ·Cytokine produced by activated CD4-positive helper T-cells and to a lesser extend activa…
  • ·cytokine activity
  • ·interleukin-2 receptor binding
  • ·adaptive immune response

Apoptosis & cell death

  • ·negative regulation of apoptotic process
  • ·negative regulation of B 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 IL2

Gene-level evidence surfaced through the gene IL2 that 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
0.80Well supported

Genetic evidence dominant · Open Targets 0.49

Hypersensitivity
0.60Moderately supported

Genetic evidence dominant · Open Targets 0.36

Rhinitis, Allergic
0.60Moderately supported

Genetic evidence dominant · Open Targets 0.36

Dermatitis, Atopic
0.58Moderately supported

Genetic evidence dominant · Open Targets 0.35

Cholangitis, Sclerosing
0.55Moderately supported

Genetic evidence dominant · Open Targets 0.29

View evidence synthesis (5)
AsthmaWell supported
0.80
agreement 0.66–0.93
Genetic87%Literature13%

Open Targets aggregate 0.49 · 2 independent evidence families

HypersensitivityModerately supported
0.60
agreement 0.46–0.74
Genetic92%Literature8%

Open Targets aggregate 0.36 · 2 independent evidence families

Rhinitis, AllergicModerately supported
0.60
agreement 0.46–0.74
Genetic91%Literature9%

Open Targets aggregate 0.36 · 2 independent evidence families

Dermatitis, AtopicModerately supported
0.58
agreement 0.44–0.72
Genetic94%Literature6%

Open Targets aggregate 0.35 · 2 independent evidence families

Cholangitis, SclerosingModerately supported
0.55
agreement 0.43–0.67
Genetic73%Animal model24%Literature3%

Open Targets aggregate 0.29 · 3 independent evidence families

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
Asthma0.49
Breast Neoplasms0.42
Hypersensitivity0.36
Rhinitis, Allergic0.36
Dermatitis, Atopic0.35
Respiratory Tract Diseases0.33
Crohn's Disease0.31
Psoriasis0.30
Cholangitis, Sclerosing0.29

Tractability

Small molecules — Emerging

Feasibility evidence (structure with ligand and high-quality ligand) — no clinical-stage drug of this modality recorded.

Antibodies — Emerging

Feasibility evidence (go cc high conf and uniprot loc med conf) — no clinical-stage drug of this modality recorded.

Protein degraders — Emerging

Feasibility evidence (small molecule binder) — no clinical-stage drug of this modality recorded.

View underlying tractability evidence (7)
SM · Structure with LigandSM · High-Quality LigandSM · Med-Quality PocketAB · GO CC high confAB · UniProt loc med confAB · UniProt SigP or TMHMMPR · Small Molecule Binder

Raw Open Targets tractability assessment buckets, by modality.

Research activity

22 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

Recent

Europe PMC papers linked directly to this protein.