CLEC5A

Description

The CLEC5A (C-type lectin domain containing 5A) is a protein-coding gene located on chromosome 7.

CLEC5A, also known as C-type lectin superfamily member 5 (CLECSF5) and myeloid DAP12-associating lectin 1 (MDL-1), is a C-type lectin that in humans is encoded by the CLEC5A gene. Structurally, MDL-1 is a type II transmembrane protein with a short cytoplasmic tail and without signaling motifs, therefore it requires association with the adaptor protein DAP12 to generate signals via Syk pathway. MDL-1 is highly expressed on myeloid lineages like neutrophil, monocyte, macrophage and also osteoclast, microglia and dendritic cells. Activation of MDL-1 induces production of many cytokines (TNF-α, IL-1, IL-6, IL-8 and IL-17A) and chemokines (MIP-1α, RANTES, IP-10, MDC). MDL-1 also amplifies innate immune response.

== Viral pathology == The most known ligand for CLEC5A is dengue virus (DV). Activated CLEC5A by binding to the dengue virion leads to phosphorylation of DAP12 and through Syk pathway are induced proinflammatory cytokines. CLEC5A is responsible for dengue virus induced hemorrhagic fever (DHF) and dengue shock syndrome (DSS), which is the most severe immune response to dengue virus infection and it is characterized by plasma leakage because of the increased vascular permeability. Interaction of CLEC5A and dengue virus also induces osteolytic activity. Another pathogen is influenza virus and its hemagglutinin protein, which interacts with CLEC5A. Through this interaction is stimulated innate immune response and it leads to secretion of proinflammatory cytokines.

CLEC5A acts as a positive regulator of osteoclastogenesis. It functions as a cell surface receptor signaling through TYROBP, and it regulates inflammatory responses.

CLEC5A is also known as CLECSF5, MDL-1, MDL1.

Associated Diseases

WES Whole Exome Sequencing