期刊名称：Proceedings of the National Academy of Sciences
印刷版ISSN：0027-8424
电子版ISSN：1091-6490
出版年度：1998
卷号：95
期号：3
页码：1160-1165
DOI：10.1073/pnas.95.3.1160
语种：English
出版社：The National Academy of Sciences of the United States of America
摘要：Ig class switching usually occurs as a consequence of cognate interactions between antigen-specific B cells and CD4+ {beta} T cells. Vesicular stomatitis virus (VSV) infection of immunocompetent mice induces a rapid T-independent neutralizing IgM response followed by a long-lived T-dependent IgG response. Surprisingly, {beta} T cell-deficient (TCR-/-) mice also produced neutralizing IgG antibodies when infected with live VSV or with a recombinant vaccinia virus expressing the VSV glycoprotein (Vacc-IND-G), but not when immunized with UV-inactivated VSV (UV-VSV). The neutralizing IgG responses did not require the presence of NK cells or complement, but were crucially dependent on IFN-{gamma} and were predominantly of the IgG2a isotype. IgG production depended on residual CD3+ non-{beta} T cell populations present in the TCR-/- mice, which produced IFN-{gamma} upon in vitro stimulation. A key role for {gamma}{delta} T cells was confirmed by the fact that TCR{beta}-/- mice also generated strong neutralizing IgG responses to VSV, whereas TCR{beta}-/-{delta}-/- mice produced very low titers. The neutralizing IgG responses of TCR-/- mice were accompanied by the development of memory B cells, but not by antigen-specific germinal center (GC) formation. Thus, during viral infection of {beta} T cell-deficient mice, {gamma}{delta} T cells may provide the signals that are required for isotype switching.
