# Unravelling mechanisms regulating Mincle activation

**Authors:** Lindsay G. Serene, Robert Buchanan, Alex J. McCarthy, Alexiane Decout

PMC · DOI: 10.1038/s42003-025-09493-8 · Communications Biology · 2026-01-08

## TL;DR

This paper reviews how Mincle, a protein involved in inflammation, is regulated and what is still unknown about its activation mechanisms.

## Contribution

The paper provides a comprehensive overview of Mincle regulation and highlights gaps for future research.

## Key findings

- Mincle is a C-type lectin that drives inflammation and binds various ligands.
- Regulatory mechanisms are essential to control Mincle activation and prevent excessive inflammation.
- Current knowledge on Mincle regulation includes its expression, ligand binding, and signaling modulation.

## Abstract

Mincle is a C-type lectin and potent driver of inflammation. Given Mincle’s ability to recognise a complex repertoire of endogenous and exogenous ligands, a network of regulatory mechanisms that precisely control Mincle activation is required to prevent excessive inflammatory responses. Here we discuss the mechanisms that govern Mincle-dependent cellular activation and the gaps in our current knowledge. Understanding the key mechanisms regulating Mincle activation could pave the way for the rational design of targeted immunotherapies and vaccines adjuvants.

This review discusses what is known about Mincle regulation: where and when it is expressed, how it binds its ligands, and the factors involved in modulating its signaling.

## Linked entities

- **Genes:** CLEC4E (C-type lectin domain family 4 member E) [NCBI Gene 26253]
- **Proteins:** CLEC4E (C-type lectin domain family 4 member E)

## Full-text entities

- **Genes:** CLEC4E (C-type lectin domain family 4 member E) [NCBI Gene 26253] {aka CLECSF9, MINCLE}
- **Diseases:** inflammation (MESH:D007249)

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12894668/full.md

## References

2 references — full list in the complete paper: https://tomesphere.com/paper/PMC12894668/full.md

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Source: https://tomesphere.com/paper/PMC12894668