Dectin 1

From WikiMD's Wellness Encyclopedia

Dectin-1 is a type of C-type lectin receptor (CLR) that plays a crucial role in the immune system by recognizing and binding to specific carbohydrate structures found on the surface of various pathogens, particularly fungi. It is encoded by the gene CLEC7A in humans.

Structure[edit | edit source]

Dectin-1 is a transmembrane protein composed of an extracellular carbohydrate recognition domain (CRD), a stalk region, a transmembrane domain, and a cytoplasmic tail. The CRD is responsible for binding to β-glucans, which are polysaccharides found in the cell walls of fungi. The cytoplasmic tail contains an immunoreceptor tyrosine-based activation motif (ITAM) that is essential for signal transduction.

Function[edit | edit source]

Dectin-1 is primarily expressed on the surface of macrophages, dendritic cells, and some neutrophils. Upon binding to β-glucans, Dectin-1 initiates a signaling cascade that leads to the activation of various immune responses, including the production of cytokines, chemokines, and the promotion of phagocytosis. This receptor is crucial for the body's defense against fungal infections, such as those caused by Candida albicans and Aspergillus fumigatus.

Signaling Pathway[edit | edit source]

The signaling pathway of Dectin-1 involves the phosphorylation of the ITAM motif by Src family kinases, which subsequently recruits and activates Syk kinase. This activation leads to the downstream activation of various signaling molecules, including NF-κB, MAPK, and CARD9, which are involved in the transcription of genes necessary for the immune response.

Clinical Significance[edit | edit source]

Mutations or deficiencies in Dectin-1 can lead to increased susceptibility to fungal infections. Research has shown that individuals with certain polymorphisms in the CLEC7A gene may have a higher risk of developing chronic mucocutaneous candidiasis. Additionally, Dectin-1 has been implicated in the pathogenesis of various inflammatory and autoimmune diseases due to its role in modulating immune responses.

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References[edit | edit source]

External Links[edit | edit source]

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Contributors: Prab R. Tumpati, MD