Publications by authors named "C R Engwerda"

Spinal cord injury (SCI) increasingly affects aged individuals, where functional impairment and mortality are highest. However, the aging-dependent mechanisms underpinning tissue damage remain elusive. Here, we find that natural killer-like T (NKLT) cells seed the intact aged human and murine spinal cord and multiply further after injury.

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Understanding the development and maintenance of immunological memory is important for efforts to eliminate parasitic diseases like leishmaniasis. Leishmaniasis encompasses a range of pathologies, resulting from infection with protozoan parasites belonging to the subgenera and of the genus A striking feature of these infections is that natural or drug-mediated cure of infection generally confers life-long protection against disease. The generation of protective T cell responses are necessary to control infections.

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Article Synopsis
  • Human immune responses to infections like malaria are influenced by genetics, environment, and past infections, but the role of latent cytomegalovirus (CMV) in malaria immunity is not well understood.
  • Research examined how CMV affects immune responses to malaria using samples from prior clinical trials, revealing that CMV seropositivity leads to lower production of specific antibodies after malaria infection and vaccination, and alters Tfh cell responses.
  • The study indicates that individuals with CMV are less likely to develop protective antibodies against malaria, highlighting the need for further research in malaria-endemic areas to understand how CMV might affect immunity in children.
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Visceral leishmaniasis is a potentially devastating neglected tropical disease caused by the protozoan parasites and (). These parasites reside in tissue macrophages and survive by deploying a number of mechanisms aimed at subverting the host immune response. CD4 T cells play an important role in controlling parasites by providing help in the form of pro-inflammatory cytokines to activate microbiocidal pathways in infected macrophages.

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Malaria, caused by infection with Plasmodium parasites, drives multiple regulatory responses across the immune landscape. These regulatory responses help to protect against inflammatory disease but may in some situations hamper the acquisition of adaptive immune responses that clear parasites. In addition, the regulatory responses that occur during Plasmodium infection may negatively affect malaria vaccine efficacy in the most at-risk populations.

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