CLEC9A is a group V CTLR (C-type lectin-like receptor) that functions as an activation receptor and is expressed on myeloid lineage cells. This protein is also expressed at the cell surface and acts as glycosylated dimers which mediate endocytosis, but not phagocytosis (Poulin LF et al, 2010). It facilitates antigen uptake and presentation, and may provide a suitable target for antibody-mediated antigen delivery. CLEC9A is important for conveying information from necrotic cells to T-cells and defines a pathway by which adaptive immune responses can be initiated in the absence of infection. It recruits Syk to mediate sensing of necrosis by the principal DC subset involved in regulating cross priming to cell-associated antigens. Signaling via this kinase occurs through a novel pathway involving CARD9 which induce a variety of cellular responses including the induction of cytokines (such as TNF, IL-6, IL-10, IL-23, and IL-2), the respiratory burst, and the production of Arachidonic acid. In addition, it also induces TH17 (T-helper type 17) adaptive responses in vivo. Expression of CLEC9A is highly restricted in peripheral blood, being detected only on BDCA3+ DCs and on a small subset of CD14+ CD16- monocytes. CLEC9A serves as a new marker to distinguish subtypes of DCs.
C-type lectin domain family 9 member A; Dendritic cell natural killer lectin group receptor 1; DNGR1; HEEE9341; UNQ9341; UNQ9341/PRO34046
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