FITC Anti-CD16 antibody [GRM1]

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Receptor for the invariable Fc fragment of immunoglobulin gamma (IgG). Optimally activated upon binding of clustered antigen-IgG complexes displayed on cell surfaces, triggers lysis of antibody-coated cells, a process known as antibody-dependent cellular cytotoxicity (ADCC). Does not bind free monomeric IgG, thus avoiding inappropriate effector cell activation in the absence of antigenic trigger (PubMed : 11711607, PubMed : 21768335, PubMed : 22023369, PubMed : 24412922, PubMed : 25786175, PubMed : 25816339, PubMed : 28652325, PubMed : 8609432, PubMed : 9242542). Mediates IgG effector functions on natural killer (NK) cells. Binds antigen-IgG complexes generated upon infection and triggers NK cell-dependent cytokine production and degranulation to limit viral load and propagation. Involved in the generation of memory-like adaptive NK cells capable to produce high amounts of IFNG and to efficiently eliminate virus-infected cells via ADCC (PubMed : 24412922, PubMed : 25786175). Regulates NK cell survival and proliferation, in particular by preventing NK cell progenitor apoptosis (PubMed : 29967280, PubMed : 9916693). Following the engagement of antigen-IgG complexes, triggers phosphorylation of immunoreceptor tyrosine-based activation motif (ITAM)-containing adapters with subsequent activation of phosphatidylinositol 3-kinase signaling and sustained elevation of intracellular calcium that ultimately drive NK cell activation. The ITAM-dependent signaling coupled to receptor phosphorylation by PKC mediates robust intracellular calcium flux that leads to production of pro-inflammatory cytokines, whereas in the absence of receptor phosphorylation it mainly activates phosphatidylinositol 3-kinase signaling leading to cell degranulation (PubMed : 1825220, PubMed : 23024279, PubMed : 2532305). Costimulates NK cells and trigger lysis of target cells independently of IgG binding (PubMed : 10318937, PubMed : 23006327). Mediates the antitumor activities of therapeutic antibodies. Upon ligation on monocytes triggers TNFA-dependent ADCC of IgG-coated tumor cells (PubMed : 27670158). Mediates enhanced opsonisation and ADCC in response to afucosylated IgGs (PubMed : 34485821, PubMed : 28566370).. (Microbial infection) Involved in Dengue virus pathogenesis via antibody-dependent enhancement (ADE) mechanism. Secondary infection with Dengue virus triggers elevated levels of afucosylated non-neutralizing IgG1s with reactivity to viral envelope/E protein. Viral antigen-IgG1 complexes bind with high affinity to FCGR3A, facilitating virus entry in myeloid cells and subsequent viral replication.

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CD16a, CD16A, FCG3, FCGR3, IGFR3, FCGR3A, Low affinity immunoglobulin gamma Fc region receptor III-A, IgG Fc receptor III-A, CD16-II, CD16a antigen, Fc-gamma RIII-alpha, FcR-10, IgG Fc receptor III-2, Fc-gamma RIII, Fc-gamma RIIIa, FcRIII, FcRIIIa, FcgammaRIIIA