{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Ross P"],"funding":["Clinical Investigation Core","Clinical Investigation Core of the UC San Diego Center for AIDS Research","NIAID NIH HHS","National Institutes of Health","NIAID","NIH HHS","UC San Diego Center for AIDS Research"],"pagination":["2180-2188"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12481035"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["214(9)"],"pubmed_abstract":["NK cells utilize effector functions, including antibody-dependent cellular cytotoxicity (ADCC), for the clearance of viral infection and cellular malignancies. While antibody-induced clustering of FcγRIIIa (CD16a) is thought to drive ADCC, the molecular basis for this activity has not been fully described. We used MINFLUX nanoscopy to map the spatial distribution of CD16a within the NK-cell ADCC immune synapse. In both resting and NK cells activated on supported lipid bilayers by Trastuzumab, we detected pairs of CD16a molecules approximately 18 nm apart that could be homodimers. NK-cell activation results in a modest increase of clusters of 4 or more CD16a localizations without a change in cluster characteristics, while CD16a pair distances do not significantly change, suggesting that sub"],"journal":["Journal of immunology (Baltimore, Md. : 1950)"],"pubmed_title":["CD16a pairs form the basal molecular subunit for the NK-cell ADCC lytic synapse."],"pmcid":["PMC12481035"],"funding_grant_id":["1R01AI167646","R01 AI167646","P30 AI036214","R01AI181784","AI036214","R01 AI181784"],"pubmed_authors":["Zwick MB","Fernandez Quintero M","Murin CD","Ross P","Cid T","Spencer K","Mace EM","Fatima H","Leaman DP","Loeffler J","Henderson SC","Matthias J","Ward AB"],"additional_accession":[]},"is_claimable":false,"name":"CD16a pairs form the basal molecular subunit for the NK-cell ADCC lytic synapse.","description":"NK cells utilize effector functions, including antibody-dependent cellular cytotoxicity (ADCC), for the clearance of viral infection and cellular malignancies. While antibody-induced clustering of FcγRIIIa (CD16a) is thought to drive ADCC, the molecular basis for this activity has not been fully described. We used MINFLUX nanoscopy to map the spatial distribution of CD16a within the NK-cell ADCC immune synapse. In both resting and NK cells activated on supported lipid bilayers by Trastuzumab, we detected pairs of CD16a molecules approximately 18 nm apart that could be homodimers. NK-cell activation results in a modest increase of clusters of 4 or more CD16a localizations without a change in cluster characteristics, while CD16a pair distances do not significantly change, suggesting that sub","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-07-15T05:53:35.265Z","creation":"2026-06-30T03:20:42.831Z"},"accession":"S-EPMC12481035","cross_references":{"pubmed":["40570099"],"doi":["10.1093/jimmun/vkaf077"]}}