Protein / target

C-C motif chemokine 17

Encoded byCCL17Q92583Homo sapiensSwiss-Prot

UniProt: Q92583 Ensembl: ENSG00000102970 HGNC: HGNC:10615 NCBI Gene: 6361

Small-molecule tractable

Druggability

Med-Quality Pocket

Research papers

Protein at a glance

Biological role

Signaling receptor binding

Strongest disease association

Cardiomyopathies

Via encoding gene CCL17 · Genetic evidence · score 0.36

Research activity

Emerging research

1 papers · latest 2021

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

Chemokine, which displays chemotactic activity for T lymphocytes, preferentially Th2 cells, but not monocytes or granulocytes.

View complete UniProt function annotation

Chemokine, which displays chemotactic activity for T lymphocytes, preferentially Th2 cells, but not monocytes or granulocytes. Therefore plays an important role in a wide range of inflammatory and immunological processes (PubMed:8702936, PubMed:9169480). Acts by binding to CCR4 at T-cell surface (PubMed:10540332, PubMed:9169480). Mediates GM-CSF/CSF2-driven pain and inflammation (PubMed:27525438). In the brain, required to maintain the typical, highly branched morphology of hippocampal microglia under homeostatic conditions. May be important for the appropriate adaptation of microglial morphology and synaptic plasticity to acute lipopolysaccharide (LPS)-induced neuroinflammation (By similarity). Plays a role in wound healing, mainly by inducing fibroblast migration into the wound (By similarity)

Subcellular location

Secreted

Domains and Gene Ontology detail (9)

Gene Ontology

Cextracellular region
Cextracellular space
Fchemokine activity
Fsignaling receptor binding
Pcell chemotaxis
Pcell-cell signaling
Pchemotaxis
Pimmune response
Pinflammatory response

94 aa · 11 kDa

Biological roles

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

Cell migrationGOImmune signallingGO

View supporting evidence

Cell migration

·cell chemotaxis
·chemotaxis

Immune signalling

·immune response
·inflammatory response

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 CCL17

Gene-level evidence surfaced through the gene CCL17 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.

Cardiomyopathies

0.36Limited support

Genetic evidence dominant · Open Targets 0.22

Lupus Erythematosus, Systemic

0.29Limited support

Genetic evidence dominant · Open Targets 0.15

Neoplasms

0.14Preliminary

Literature evidence dominant · Open Targets 0.11 · no direct causal or clinical evidence

Lung Diseases, Interstitial

0.13Preliminary

Literature evidence dominant · Open Targets 0.10 · no direct causal or clinical evidence

Idiopathic Pulmonary Fibrosis

0.13Preliminary

Literature evidence dominant · Open Targets 0.10 · no direct causal or clinical evidence

View evidence synthesis (5)

CardiomyopathiesLimited support

0.36

agreement 0.22–0.50

Genetic100%Literature1%

Open Targets aggregate 0.22 · 2 independent evidence families

Lupus Erythematosus, SystemicLimited support

0.29

agreement 0.15–0.43

Genetic69%Literature32%

Open Targets aggregate 0.15 · 2 independent evidence families

NeoplasmsPreliminary

0.14

agreement 0.00–0.41

Literature100%

Open Targets aggregate 0.11 · 1 independent evidence family · no direct causal or clinical evidence

Lung Diseases, InterstitialPreliminary

0.13

agreement 0.00–0.40

Literature100%

Open Targets aggregate 0.10 · 1 independent evidence family · no direct causal or clinical evidence

Idiopathic Pulmonary FibrosisPreliminary

0.13

agreement 0.00–0.32

Literature98%RNA expression2%

Open Targets aggregate 0.10 · 2 independent evidence families · no direct causal or clinical evidence

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

Cardiomyopathies0.22

Lupus Erythematosus, Systemic0.15

Neoplasms0.11

Lung Diseases, Interstitial0.10

Idiopathic Pulmonary Fibrosis0.10

Familial prostate cancer0.09

Prostatic Neoplasms0.09

Prostate carcinoma0.09

Alzheimer's Disease0.09

Esophageal Squamous Cell Carcinoma0.08

Tractability

Small molecules — Emerging

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

Antibodies — Emerging

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

View underlying tractability evidence (4)

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

Raw Open Targets tractability assessment buckets, by modality.

Research activity

1 papers · to 2021

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

Most cited

Biomarkers in atopic dermatitis-a review on behalf of the International Eczema Council.252 cites

Renert-Yuval Y · The Journal of allergy and clinical immunology · 2021

Recent

Biomarkers in atopic dermatitis-a review on behalf of the International Eczema Council.

Renert-Yuval Y · The Journal of allergy and clinical immunology · 2021

Europe PMC papers linked directly to this protein.