Correction to: T follicular helper expansion and humoral-mediated rejection are independent of the HVEM/BTLA pathway.

In this article, one of the grating agencies requested us to incorporate the information, Spanish Government and co-funded by European Union ERDF/ESF, "Investing in your future", in the acknowledgments section. The correct acknowledgement is as follows: "This work has been supported by grants of the Spanish Ministry of Health (Fondo de Investigaciones Sanitarias, PI13/00029, Spanish Government and co-funded by European Union ERDF/ESF, "Investing in your future"), Department of Education of Castilla and Leon Regional Government (Grant# LE093U13) and Mutua Madrileña Foundation (Basic research grants 2012) to J.I.R.B.; by Miguel Servet National Program (Ministry of National Health) CP12/03063 and by Gerencia Regional de Salud GRS963/A/2014 to M.L.R.G. We are particularly grateful to Mr. Leonides Alaiz for outstanding animal husbandry." The authors regret the errors.

T follicular helper expansion and humoral-mediated rejection are independent of the HVEM/BTLA pathway.

The molecular pathways contributing to humoral-mediated allograft rejection are poorly defined. In this study, we assessed the role of the herpesvirus entry mediator/B- and T-lymphocyte attenuator (HVEM/BTLA) signalling pathway in the context of antibody-mediated allograft rejection. An experimental setting was designed to elucidate whether the blockade of HVEM/BTLA interactions could modulate de novo induction of host antidonor-specific antibodies during the course of graft rejection. To test this hypothesis, fully allogeneic major histocompatibility complex-mismatched skin grafts were transplanted onto the right flank of recipient mice that were treated with isotype control, anti-CD40L or modulatory antibodies of the HVEM/BTLA signalling pathway. The frequencies of CD4 T follicular helper (Tfh) cells (B220-, CD4+ CXCR5+ PD-1high), extrafollicular helper cells (B220-, CD4+ CXCR5- PD-1+ and PD-1-) and germinal centre (GC) B cells (B220+Fas+ GL7+) were analysed by flow cytometry in draining and non-draining lymph nodes at day 10 post transplantation during the acute phase of graft rejection. The host antidonor isotype-specific humoral immune response was also assessed. Whereas blockade of the CD40/CD40L pathway was highly effective in preventing the allogeneic humoral immune response, antibody-mediated blockade of the HVEM/BTLA-interacting pathway affected neither the expansion of Tfh cells nor the expansion of GC B cells. Consequently, the course of the host antidonor antibody-mediated response proceeded normally, without detectable evidence of impaired development. In summary, these data indicate that HVEM/BTLA interactions are dispensable for the formation of de novo host antidonor isotype-specific antibodies in transplantation.