Szomolanyi-Tsuda, EvaBrien, James D.Dorgan, Jill E.Welsh, Raymond M.Garcea, Robert L.2022-08-232022-08-232000-05-232009-03-10<p>J Immunol. 2000 Jun 1;164(11):5877-82.</p>0022-1767 (Print)10.4049/jimmunol.164.11.587710820268https://hdl.handle.net/20.500.14038/38259Polyomavirus (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.en-USAnimalsAntibodies, ViralAntigens, CD40Antigens, T-IndependentB-LymphocytesCD40 LigandCapsid*Capsid ProteinsGenes, T-Cell Receptor betaGenes, T-Cell Receptor deltaImmunoglobulin GLigandsLymphopeniaMembrane GlycoproteinsMiceMice, Inbred C57BLMice, KnockoutMice, SCIDPolyomavirusPolyomavirus InfectionsT-LymphocytesTumor Virus InfectionsLife SciencesMedicine and Health SciencesJournal Articlehttps://escholarship.umassmed.edu/oapubs/1132770110oapubs/1132