BDCA2 (blood dendritic cell antigen 2), also known as CD303 or CLEC4C, is a C-type lectin receptor selectively expressed on human plasmacytoid dendritic cells (pDCs) and functions as a regulator of innate immune signaling
[1][2]. BDCA2 contains an immunoreceptor tyrosine-based activation motif (ITAM)-like signaling domain and transduces signals through associated Fc receptor γ chain (FcRγ), leading to modulation of intracellular signaling pathways
[2][3]. Mechanistically, BDCA2 engagement induces phosphorylation-dependent signaling that suppresses Toll-like receptor (TLR) 7- and TLR9-mediated type I interferon production by pDCs
[3][4]. In disease models, BDCA2-mediated regulation of pDC activation has been investigated in autoimmune diseases, particularly systemic lupus erythematosus (SLE), where excessive type I interferon responses contribute to disease pathology
[4][5]. BDCA2 activation reduces pDC-derived interferon-α production and inflammatory cytokine responses, supporting its role as a regulatory checkpoint of pDC immune function
[3][5]. Compared with related C-type lectin receptors expressed on immune cells, BDCA2 shows restricted expression on pDCs and serves as a characteristic surface marker for human pDC identification
[1][2]. Unlike BDCA4/CD304, another pDC-associated marker involved in cell surface identification, BDCA2 directly regulates pDC signaling through ITAM-associated pathways
[2][6]. For experimental applications, BDCA2 is studied using antibody-mediated receptor crosslinking, pDC activation assays, and analysis of interferon responses
[3][5]. BDCA2-targeting antibodies have been developed as experimental tools and therapeutic candidates to investigate pDC-driven immune activation and interferon-related diseases
[5][7].