English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

CD8 +  T cells are key players during infection with the malaria parasite  Plasmodium berghei  ANKA (PbA). While they cannot provide protection against blood-stage parasites, they can cause immunopathology, thus leading to the severe manifestation of cerebral malaria. Hence, the tight control of CD8 +  T cell function is key in order to prevent fatal outcomes. One major mechanism to control CD8 +  T cell activation, proliferation and effector function is the integration of co-inhibitory and co-stimulatory signals. In this study, we show that one such pathway, the HVEM-CD160 axis, significantly impacts CD8 +  T cell regulation and thereby the incidence of cerebral malaria. Here, we show that the co-stimulatory molecule HVEM is indeed required to maintain CD8 +  T effector populations during infection. Additionally, by generating a CD160 −/−  mouse line, we observe that the HVEM ligand CD160 counterbalances stimulatory signals in highly activated and cytotoxic CD8 +  T effector cells, thereby restricting immunopathology. Importantly, CD160 is also induced on cytotoxic CD8 +  T cells during acute  Plasmodium falciparum  malaria in humans. In conclusion, CD160 is specifically expressed on highly activated CD8 +  T effector cells that are harmful during the blood-stage of malaria.

HVEM and CD160: Regulators of Immunopathology During Malaria Blood-Stage