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.

Modulation of cytotoxic responses by targeting CD160 prolongs skin graft survival across major histocompatibility class I barrier.

CD160 is a glycosylphosphatidylinositol-anchored protein of the immunoglobulin superfamily. It exhibits a pattern of expression coincident in humans and mice that is mainly restricted to cytotoxic cells and to all intestinal intraepithelial T lymphocytes. B- and T-lymphocyte attenuator (BTLA) and CD160 interact with cysteine-rich domain 1 of the extracellular region of Herpesvirus entry mediator (HVEM).

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.

Immunotherapeutic targeting of LIGHT/LTβR/HVEM pathway fully recapitulates the reduced cytotoxic phenotype of LIGHT-deficient T cells.

Tumor necrosis factor (TNF)/TNF receptor (TNFR) superfamily members play essential roles in the development of the different phases of the immune response. Mouse LIGHT (TNFSF14) is a type II transmembrane protein with a C-terminus extracellular TNF homology domain (THD) that assembles in homotrimers and regulates the course of the immune responses by signaling through 2 receptors, the herpes virus entry mediator (HVEM, TNFRSF14) and the lymphotoxin β receptor (LTβR, TNFRSF3). LIGHT is a membrane-bound protein transiently expressed on activated T cells, natural killer (NK) cells and immature dendritic cells that can be proteolytically cleaved by a metalloprotease and released to the extracellular milieu.

Clinical evolution of chronic renal patients with HIV infection in replacement therapy.

Patients on renal replacement therapy (RRT) infected with the human immunodeficiency virus (HIV) are a special group with growing interest. In order to study the epidemiological data of HIV+ patients on RRT in Spain, we collected individual information from 2004-2011 (period of use of highly active antiretroviral therapy [HAART] in the Autonomous Communities of Andalusia, Aragon, Asturias, Catalonia, Valencia, Castilla la Mancha, Castilla León, Galicia, Madrid, La Rioja and the Basque Country, comprising 85% of the Spanish population. A total of 271 incident and 209 prevalent patients were analysed.