Recher, M.Lang, K. S.Hunziker, L.Freigang, S.Eschli, B.Harris, N. L.Navarini, A.Senn, B. M.Fink, K.Lotscher, M.Hangartner, L.Zellweger, R.Hersberger, M.Theocharides, A.Hengartner, H.Zinkernagel, R. M.2010-01-062010-01-062010-01-06200410.1038/ni1102https://infoscience.epfl.ch/handle/20.500.14299/45069The B cell response to lymphocytic choriomeningitis virus is characterized by a CD4(+) T cell-dependent polyclonal hypergammaglobulinemia and delayed formation of virus-specific neutralizing antibodies. Here we provide evidence that, paradoxically, because of polyclonal B cell activation, virus-specific T cell help impairs the induction of neutralizing antibody responses. Experimental reduction in CD4(+) T cell help in vivo resulted in potent neutralizing antibody responses without impairment of CD8(+) T cell activity. These unexpected consequences of polyclonal B cell activation may affect vaccine strategies and the treatment of clinically relevant chronic bacterial, parasitic and viral infections in which hypergammaglobulinemia is regularly found.AnimalsAntibody Formation/*immunologyArenaviridae Infections/immunologyB-Lymphocytes/*immunologyCD4-Positive T-Lymphocytes/*immunologyEnzyme-Linked Immunosorbent AssayFlow CytometryLymphocyte Activation/*immunologyLymphocytic choriomeningitis virus/immunologyMicetext::journal::journal article::research article