Expansion of Murine Gammaherpesvirus Latently Infected B Cells Requires T Follicular Help

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During an immune response, B cells respond to invading pathogens by undergoing massive expansion during the germinal center reaction. This proliferation requires signals from CD4 T cells, with some B cells then maturing into antibody secreting plasma cells, while others mature into memory B cells that may persist for the life of the host. Gammaherpesviruses take advantage of this immune response by infecting B cells, resulting in expansion of the pool of infected cells during the germinal center reaction. The human gammaherpesvirus Epstein-Barr virus (EBV) is thought to be able to accomplish this without the need for CD4 T cell help by expressing viral proteins that mimic signals from CD4 T cells. Here we show in a mouse model of gammaherpesvirus infection that infected B cells require signals from CD4 T cells for proliferation. Since the mouse gammaherpesvirus and EBV belong to different subgroups of gammaherpesviruses, this suggests that these subgroups utilize fundamentally different strategies to expand the pool of infected B cells during the establishment of latency. These different strategies may explain the different outcome of infection by these different subgroups of gammaherpesviruses in the context of defective germinal center responses that result from defective CD4 T cell help.

Vyšlo v časopise: Expansion of Murine Gammaherpesvirus Latently Infected B Cells Requires T Follicular Help. PLoS Pathog 10(5): e32767. doi:10.1371/journal.ppat.1004106
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1004106

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