B-lymphocyte antigen CD20 and Low affinity immunoglobulin gamma Fc receptor III-A complex (CD20-Rituximab-FcγRIIIa)

The CD20–rituximab–FcγRIIIa immunological synapse is a specialized intercellular junction formed between a CD20-positive B cell and a Natural Killer (NK) cell, bridged by the therapeutic monoclonal antibody rituximab. Rituximab binds to the CD20 antigen (MS4A1) on the B cell surface via its Fab regions, while its Fc region engages the FcγRIIIa (CD16a/FCGR3A) receptor on the NK cell (UniProt P11836, P08637). This ternary interaction triggers the polarization of the NK cell's cytotoxic machinery toward the B cell, leading to the release of perforin and granzymes in a process known as antibody-dependent cellular cytotoxicity (ADCC) (PubMed PMID: 32054756). This synapse is the fundamental structural unit through which rituximab exerts its anti-tumor and B-cell depleting effects in the treatment of non-Hodgkin lymphomas, chronic lymphocytic leukemia, and various autoimmune disorders (DrugBank DB00073). The efficiency and stability of this synapse are critical determinants of therapeutic efficacy and can be influenced by factors such as CD20 density and genetic polymorphisms in the FCGR3A gene.

Other names

CD20-CD16a synapseRituximab-mediated immunological synapseADCC synapseCD20-Rituximab-CD16a complexMS4A1-FCGR3A complex

Rituximab binds to CD20 on B cells and recruits NK cells via the FcγRIIIa receptor to induce antibody-dependent cellular cytotoxicity (ADCC).