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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 IL2that 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 0.660.93
Genetic87%Literature13%

Open Targets aggregate 0.49 · 2 independent evidence families

HypersensitivityModerately supported
0.60
agreement 0.460.74
Genetic92%Literature8%

Open Targets aggregate 0.36 · 2 independent evidence families

Rhinitis, AllergicModerately supported
0.60
agreement 0.460.74
Genetic91%Literature9%

Open Targets aggregate 0.36 · 2 independent evidence families

Dermatitis, AtopicModerately supported
0.58
agreement 0.440.72
Genetic94%Literature6%

Open Targets aggregate 0.35 · 2 independent evidence families

Cholangitis, SclerosingModerately supported
0.55
agreement 0.430.67
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 moleculesEmerging

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

AntibodiesEmerging

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

Protein degradersEmerging

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.