Dendritic cell-specific surface receptor (DCSR) (DCSR)

Dendritic cell-specific surface receptors are a diverse group of proteins, primarily belonging to the C-type lectin receptor (CLR) family, that are expressed on the surface of dendritic cells (DCs) to facilitate their role as the primary initiators of the adaptive immune response (Figdor et al., 2002, Nature Reviews Immunology). These receptors, including DC-SIGN (CD209), DEC-205 (CD205), and BDCA-2 (CD303), are specialized in recognizing and internalizing a wide array of pathogens and self-antigens through specific carbohydrate recognition domains (Geijtenbeek & Gringhuis, 2009, Nature Reviews Immunology). Once bound, these receptors mediate the endocytosis of antigens, which are then processed and presented on MHC molecules to T cells, effectively bridging innate and adaptive immunity (Steinman, 2012, Annual Review of Immunology). In therapeutic applications, these receptors are targeted to enhance vaccine efficacy by conjugating antigens to receptor-specific antibodies, ensuring efficient delivery to DCs (Tacken et al., 2007, Nature Reviews Immunology). Conversely, certain pathogens like HIV-1 exploit these receptors to facilitate viral dissemination, and overactivity of specific receptors like BDCA-2 is implicated in autoimmune diseases such as systemic lupus erythematosus (Furie et al., 2019, NEJM). Consequently, these receptors are significant targets for both immune-stimulatory therapies in cancer and immune-modulatory treatments in chronic inflammation and infection.

Other names

Dendritic cell receptorsDC surface markersC-type lectin receptors on DCsDC-specific C-type lectinsDendritic cell-specific surface receptors

The mechanism of action involves the use of monoclonal antibodies or antibody-drug conjugates to either agonize receptors for antigen uptake and presentation (e.g., DEC-205 targeting in vaccines) or to antagonize receptors to inhibit inflammatory signaling (e.g., BDCA-2 inhibition in lupus) (Tacken et al., 2007, Nature Reviews Immunology; Furie et al., 2019, NEJM).