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dc.contributor.authorSzomolanyi-Tsuda, Eva
dc.contributor.authorBrien, James D.
dc.contributor.authorDorgan, Jill E.
dc.contributor.authorWelsh, Raymond M.
dc.contributor.authorGarcea, Robert L.
dc.date2022-08-11T08:09:31.000
dc.date.accessioned2022-08-23T16:34:06Z
dc.date.available2022-08-23T16:34:06Z
dc.date.issued2000-05-23
dc.date.submitted2009-03-10
dc.identifier.citation<p>J Immunol. 2000 Jun 1;164(11):5877-82.</p>
dc.identifier.issn0022-1767 (Print)
dc.identifier.doi10.4049/jimmunol.164.11.5877
dc.identifier.pmid10820268
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38259
dc.description.abstractPolyomavirus (PyV) infection elicits protective T cell-independent (TI) IgG responses in T cell-deficient mice. The question addressed in this report is whether CD40 signaling plays a role in this TI antiviral IgG response. Because CD40 ligand (CD40L) can be expressed on numerous cell types in addition to activated T cells, it is possible that cells other than T cells provide CD40L to signal through CD40 on B cells and hence positively influence the antiviral TI IgG responses. In this study we show, by blocking CD40-CD40L interactions in vivo with anti-CD40L Ab treatment in TCR betaxdelta-/- mice and by using SCID mice reconstituted with CD40-/- B cells, that the lack of CD40 signaling in B cells results in a 50% decrease in TI IgG secreted in response to PyV. SCID mice reconstituted with CD40L-/- B cells also responded to PyV infection with diminished IgG secretion compared with that of SCID mice reconstituted with wild-type B cells. This finding suggests that B cells may provide the CD40L for CD40 signaling in the absence of T cell help during acute virus infection. Our studies demonstrate that, although about half of the TI IgG responses to PyV are independent of CD40-CD40L interactions, these interactions occur in T cell-deficient mice and enhance antiviral TI Ab responses.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=10820268&dopt=Abstract">Link to Article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.4049/jimmunol.164.11.5877
dc.subjectAnimals
dc.subjectAntibodies, Viral
dc.subjectAntigens, CD40
dc.subjectAntigens, T-Independent
dc.subjectB-Lymphocytes
dc.subjectCD40 Ligand
dc.subjectCapsid
dc.subject*Capsid Proteins
dc.subjectGenes, T-Cell Receptor beta
dc.subjectGenes, T-Cell Receptor delta
dc.subjectImmunoglobulin G
dc.subjectLigands
dc.subjectLymphopenia
dc.subjectMembrane Glycoproteins
dc.subjectMice
dc.subjectMice, Inbred C57BL
dc.subjectMice, Knockout
dc.subjectMice, SCID
dc.subjectPolyomavirus
dc.subjectPolyomavirus Infections
dc.subjectT-Lymphocytes
dc.subjectTumor Virus Infections
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleThe role of CD40-CD154 interaction in antiviral T cell-independent IgG responses
dc.typeJournal Article
dc.source.journaltitleJournal of immunology (Baltimore, Md. : 1950)
dc.source.volume164
dc.source.issue11
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/1132
dc.identifier.contextkey770110
html.description.abstract<p>Polyomavirus (PyV) infection elicits protective T cell-independent (TI) IgG responses in T cell-deficient mice. The question addressed in this report is whether CD40 signaling plays a role in this TI antiviral IgG response. Because CD40 ligand (CD40L) can be expressed on numerous cell types in addition to activated T cells, it is possible that cells other than T cells provide CD40L to signal through CD40 on B cells and hence positively influence the antiviral TI IgG responses. In this study we show, by blocking CD40-CD40L interactions in vivo with anti-CD40L Ab treatment in TCR betaxdelta-/- mice and by using SCID mice reconstituted with CD40-/- B cells, that the lack of CD40 signaling in B cells results in a 50% decrease in TI IgG secreted in response to PyV. SCID mice reconstituted with CD40L-/- B cells also responded to PyV infection with diminished IgG secretion compared with that of SCID mice reconstituted with wild-type B cells. This finding suggests that B cells may provide the CD40L for CD40 signaling in the absence of T cell help during acute virus infection. Our studies demonstrate that, although about half of the TI IgG responses to PyV are independent of CD40-CD40L interactions, these interactions occur in T cell-deficient mice and enhance antiviral TI Ab responses.</p>
dc.identifier.submissionpathoapubs/1132
dc.contributor.departmentDepartment of Pathology
dc.source.pages5877-82


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