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Human IgG Fc receptor II mediates antibody-dependent enhancement of dengue virus infection

dc.contributor.authorLittaua, Rebecca A.
dc.contributor.authorKurane, Ichiro
dc.contributor.authorEnnis, Francis A.
dc.date2022-08-11T08:09:10.000
dc.date.accessioned2022-08-23T16:19:45Z
dc.date.available2022-08-23T16:19:45Z
dc.date.issued1990-04-15
dc.date.submitted2017-11-20
dc.identifier.citationJ Immunol. 1990 Apr 15;144(8):3183-6.
dc.identifier.issn0022-1767 (Linking)
dc.identifier.pmid2139079
dc.identifier.urihttp://hdl.handle.net/20.500.14038/35126
dc.description.abstractIt is known that anti-dengue virus antibodies at subneutralizing concentrations augment dengue virus infection of IgG FcR (Fc gamma R)-positive cells, and this phenomenon is called antibody-dependent enhancement. This is caused by the uptake of dengue virus-antibody complexes by Fc gamma R. We previously reported that Fc gamma RI can mediate antibody-dependent enhancement. In this study we use an erythroleukemia cell line, K562, which has Fc gamma RII, but does not have Fc gamma RI or Fc gamma RIII, to determine if Fc gamma RII can mediate infection by dengue virus-antibody complexes. Polyclonal mouse anti-dengue virus antibody significantly augments dengue virus infection of K562 cells, whereas normal mouse serum does not. A mAb IV.3, which is specific for Fc gamma RII and is known to inhibit the binding of Ag-antibody complex to Fc gamma RII, inhibits dengue antibody-mediated augmentation of dengue virus infection. It has been reported that Fc gamma RII binds to mouse IgG1, but not to mouse IgG2a. A mouse IgG1 anti-dengue virus mAb (3H5) augments dengue virus infection of K562 cells, but a mouse IgG2a anti-dengue virus mAb (4G2) does not. 4G2 augments dengue virus infection of a human monocytic cell line, U937, which has Fc gamma RI. Based on these results we conclude that Fc gamma RII mediate antibody-dependent enhancement of dengue virus infection in addition to Fc gamma RI.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=2139079&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://www.jimmunol.org/content/144/8/3183
dc.subjectImmunity
dc.subjectImmunology and Infectious Disease
dc.subjectImmunology of Infectious Disease
dc.subjectInfectious Disease
dc.subjectVirology
dc.titleHuman IgG Fc receptor II mediates antibody-dependent enhancement of dengue virus infection
dc.typeJournal Article
dc.source.journaltitleJournal of immunology (Baltimore, Md. : 1950)
dc.source.volume144
dc.source.issue8
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/infdis_pp/334
dc.identifier.contextkey11095261
html.description.abstract<p>It is known that anti-dengue virus antibodies at subneutralizing concentrations augment dengue virus infection of IgG FcR (Fc gamma R)-positive cells, and this phenomenon is called antibody-dependent enhancement. This is caused by the uptake of dengue virus-antibody complexes by Fc gamma R. We previously reported that Fc gamma RI can mediate antibody-dependent enhancement. In this study we use an erythroleukemia cell line, K562, which has Fc gamma RII, but does not have Fc gamma RI or Fc gamma RIII, to determine if Fc gamma RII can mediate infection by dengue virus-antibody complexes. Polyclonal mouse anti-dengue virus antibody significantly augments dengue virus infection of K562 cells, whereas normal mouse serum does not. A mAb IV.3, which is specific for Fc gamma RII and is known to inhibit the binding of Ag-antibody complex to Fc gamma RII, inhibits dengue antibody-mediated augmentation of dengue virus infection. It has been reported that Fc gamma RII binds to mouse IgG1, but not to mouse IgG2a. A mouse IgG1 anti-dengue virus mAb (3H5) augments dengue virus infection of K562 cells, but a mouse IgG2a anti-dengue virus mAb (4G2) does not. 4G2 augments dengue virus infection of a human monocytic cell line, U937, which has Fc gamma RI. Based on these results we conclude that Fc gamma RII mediate antibody-dependent enhancement of dengue virus infection in addition to Fc gamma RI.</p>
dc.identifier.submissionpathinfdis_pp/334
dc.contributor.departmentDepartment of Medicine, Division of Infectious Diseases and Immunology
dc.contributor.departmentCenter for Infectious Disease and Vaccine Research
dc.source.pages3183-6


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