Target intelligence / Profile preview

T cell-interacting, activating receptor on myeloid cells 1 (TARM1)

Target
TARM1
Molecular classification
Receptor, Immunoglobulin-like receptor family, Leukocyte immunoglobulin-like receptor family
01

Overview

T cell-interacting, activating receptor on myeloid cells 1 (TARM1) is a member of the leukocyte immunoglobulin-like receptor family, characterized by two extracellular immunoglobulin-like domains, a transmembrane domain, and a short cytoplasmic tail without a canonical signaling motif. TARM1 associates with the Fc receptor γ-chain, enabling immunoreceptor tyrosine-based activation motif (ITAM)-dependent signaling. It is primarily expressed in granulocyte/monocyte lineages, notably in granulocyte-macrophage colony-stimulating factor (GM-CSF)-induced dendritic cells, with expression upregulated during inflammatory conditions. TARM1 enhances dendritic cell maturation and antigen presentation by interacting with type II collagen, acts as a co-stimulatory molecule in myeloid cells, and is implicated in the promotion of inflammatory responses, including those seen in autoimmune arthritis. TARM1 deficiency impairs dendritic cell function and reduces disease severity in experimental autoimmune models, making it a candidate therapeutic target for modulating immune responses in autoimmune and inflammatory diseases

Other names
T-cell-interacting, activating receptor on myeloid cells protein 1OLT-2OSCAR-like transcript-2 proteinTARM1OLT-2 protein
02

Mechanism of action

Modulation of dendritic cell maturation and antigen-presenting capacity via ligand engagement (type II collagen) and FcRγ signaling\nPotential negative regulation of CD4+ T cell proliferation by binding unknown ligand on T cells

03

Biological functions

Immune responseRegulation of dendritic cell maturationAntigen presentationNegative regulation of CD4+ T cell activationStimulation of pro-inflammatory cytokine production (e.g., TNF, IL-6) by myeloid cells
04

Disease associations

Autoimmune disease (notably arthritis, including rheumatoid arthritis)InflammationPotentially infection (via regulation of myeloid cell responses)
05

Safety considerations

Potential for immune suppression or unintended immune activation if targeted therapeutically, given its role in dendritic cell activation and T cell responsesAlteration of TARM1 function may impact pro-inflammatory cytokine production and susceptibility to immune-related disorders
06

Biomarkers

Increased TARM1 expression may correlate with inflammatory dendritic cell states or autoimmune process activity (e.g., rheumatoid arthritis models)

Beyond the preview

Go deeper on T cell-interacting, activating receptor on myeloid cells 1 (TARM1).

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 T cell-interacting, activating receptor on myeloid cells 1 (TARM1).

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