Target intelligence / Profile preview

Macrophage inflammatory protein 3 alpha (MIP-3α)

Target
MIP-3α
Molecular classification
Chemokine, CC chemokine family, Cytokine, Secreted protein
01

Overview

Macrophage inflammatory protein 3 alpha (MIP-3α; also known as CCL20 or LARC) is a small secreted chemokine belonging to the CC chemokine family[1][4][6]. It consists of 70 amino acids and features a typical chemokine structure, including three β strands and a C-terminal α helix, stabilized by two disulfide bonds[1][3][7]. MIP-3α is primarily produced by mucosal and skin epithelial cells in response to inflammatory stimuli; its expression is downregulated by anti-inflammatory cytokines such as IL-10[4]. It functions as a chemoattractant for memory T cells, natural killer cells, immature dendritic cells, and Th17 cells, serving a central role in both innate and adaptive immunity[1][2][4]. Its only known receptor is CCR6, a G protein-coupled receptor[1][3][4]. Beyond chemotaxis, MIP-3α exhibits direct antimicrobial activity against bacteria such as E. coli and S. aureus, and moderate antiviral properties[1][3]. MIP-3α/CCL20 levels are associated with disease states including cancer, rheumatoid arthritis, and HIV infection, and may serve as a biomarker of immune activity in certain conditions[1][5].

Other names
CCL20LARC (liver and activation-regulated chemokine)Macrophage inflammatory protein-3α
02

Mechanism of action

Drugs targeting this molecule would typically act by blocking its interaction with CCR6 (chemokine receptor 6), disrupting lymphocyte and dendritic cell trafficking. Potential immunomodulation or suppression of chronic inflammatory signals.

03

Biological functions

Immune responseChemotaxis (recruitment of lymphocytes, dendritic cells)Antimicrobial activity (against bacteria and some viruses)Regulation of inflammationAdaptive and innate immunity
04

Disease associations

CancerInflammation (including rheumatoid arthritis and diseased periodontal tissues)Infection (notably HIV)Other immune-related diseases
05

Safety considerations

Targeting MIP-3α/CCR6 could lead to impaired immune surveillance or increased susceptibility to infection due to its key roles in recruiting immune cells and mediating the antimicrobial response[1][5].
06

Interacting drugs

No specific approved small molecules or biologics directly listed as targeting MIP-3α or CCL20 in the provided sources. Antagonists of its receptor CCR6 may be under investigation in research contexts, especially for inflammation and autoimmune disorders[1][4].
07

Biomarkers

Elevated serum levels of MIP-3α/CCL20 may be used as a biomarker in HIV infection and potentially in inflammatory diseases[5].

Beyond the preview

Go deeper on Macrophage inflammatory protein 3 alpha (MIP-3α).

Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.

Drug pipeline

Full profile access

Explore the programs pursuing this target and their development progress.

  • Drug candidates
  • Developers
  • Development stage

Clinical trials

Full profile access

Follow the clinical studies evaluating therapies directed at this target.

  • Trial design
  • Status
  • Readouts

Competitive landscape

Full profile access

Compare approaches across drug candidates, modalities, and indications.

  • Programs
  • Modalities
  • Indications

Literature & evidence

Full profile access

Investigate the research and source evidence behind target biology and development.

  • Publications
  • Sources
  • Analysis

Patents

Full profile access

Explore patent activity around therapies and technologies addressing this target.

  • Patents
  • Assignees
  • Technologies

Research & analysis

Full profile access

Connect target biology, drug development, and emerging evidence in your research.

  • Biology
  • Development news
  • Analysis

Bring the full picture into focus.

See how Gosset can support your research on Macrophage inflammatory protein 3 alpha (MIP-3α).

Explore the full profile

Gosset Free

Get started with Gosset.

Enter your work email and we’ll be in touch with next steps.

Work email preferred.

Book a call