Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Malaria is caused by apicomplexan parasites of the genus Plasmodium. While infection continues to pose a risk for the majority of the global population, the burden of disease mainly resides in Sub-Saharan Africa. Although immunity develops against disease, this requires years of persistent exposure and is not associated with protection against infection. Repeat infections occur due to the parasite's ability to disrupt or evade the host immune responses. However, despite many years of study, the mechanisms of this disruption remain unclear. Previous studies have demonstrated a parasite-induced failure in dendritic cell (DCs) function affecting the generation of helper T cell responses. These T cells fail to help B cell responses, reducing the production of antibodies that are necessary to control malaria infection. This review focuses on our current understanding of the effect of Plasmodium parasite on DC function, DC-T cell interaction, and T cell activation. A better understanding of how parasites disrupt DC-T cell interactions will lead to new targets and approaches to reinstate adaptive immune responses and enhance parasite immunity.

Original publication

DOI

10.3389/fimmu.2020.01597

Type

Journal

Frontiers in immunology

Publication Date

01/2020

Volume

11

Addresses

Institute of Infection, Immunity & Inflammation, University of Glasgow, Glasgow, United Kingdom.

Keywords

Liver, Dendritic Cells, T-Lymphocyte Subsets, T-Lymphocytes, Skin, Animals, Humans, Plasmodium, Malaria, Disease Models, Animal, Cell Communication, Immune Tolerance, Life Cycle Stages, Host-Parasite Interactions, Immunomodulation, Immune Evasion