Target intelligence / Profile preview

C-type lectin domain family 2 member D (CLEC2D)

Target
CLEC2D
Molecular classification
C-type lectin-like receptor, Transmembrane signaling receptor, Immune receptor
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Overview

C-type lectin domain family 2 member D (CLEC2D) is a type II transmembrane C-type lectin-like receptor mainly expressed on activated antigen-presenting cells such as B cells, dendritic cells, and subsets of T lymphocytes[2][3][1]. CLEC2D encodes the LLT1 (lectin-like transcript 1) protein, the only functional ligand for CD161 (NKR-P1A) on human NK and T cells[2][1]. Engagement of LLT1 with CD161 modulates immune responses by inhibiting NK cell cytotoxicity and cytokine production, and can costimulate T cell activation under certain conditions, leading to increased inflammatory cytokine release[2]. Increased LLT1 expression on tumor cells has been implicated in immune evasion during cancer, particularly by suppressing NK cell function[2][3]. CLEC2D also inhibits osteoclast formation, contributing to bone homeostasis, and may function as a pattern recognition receptor recognizing histone sequences released from necrotic cells, thus initiating sterile inflammatory responses[1][2]. CLEC2D/LLT1 is under study as a potential therapeutic target in cancer, autoimmunity, and inflammatory diseases due to its regulatory role in both innate and adaptive immunity[2][4][3][1].

Other names
LLT1OCILCLAXLectin-like NK cell receptorLectin-like transcript 1Osteoclast inhibitory lectinC-type lectin related f
02

Mechanism of action

Inhibition or modulation of NK-cell mediated lysis via engagement of LLT1 (CLEC2D) on target cells with CD161 (NKR-P1A) on NK and T cells Modulation of cytokine release via receptor-ligand engagement

03

Biological functions

Immune responseRegulation of NK cell cytotoxicity and cytokine productionT cell activation modulationInhibition of osteoclast formationBone homeostasis
04

Disease associations

Cancer (evasion of NK cell immunity, e.g., prostate cancer)InflammationAutoimmunityInfectionBone disorders (linked to osteoclast activity regulation)
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Safety considerations

Potential for immune suppression or overactivation if targeted therapeutically, given its role regulating NK and T cell activityPossible impacts on bone health if osteoclast inhibition is dysregulated

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