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Cytotoxic activities of CD8⁺ T cells collaborate with macrophages to protect against blood-stage murine malaria. | LitMetric

AI Article Synopsis

  • The role of CD8(+) T cells in protecting against blood-stage malaria is debated, particularly due to the absence of MHC class I molecules on infected human red blood cells.
  • Research shows that rodent malaria parasites can infect erythroblasts that do express MHC class I, allowing CD8(+) T cells to recognize and respond to the infection.
  • The study reveals that CD8(+) T cells use Fas ligand to trigger the death of infected erythroblasts, promoting phagocytosis of these cells through mechanisms involving phosphatidylserine and the Tim-4 receptor.

Article Abstract

The protective immunity afforded by CD8(+) T cells against blood-stage malaria remains controversial because no MHC class I molecules are displayed on parasite-infected human erythrocytes. We recently reported that rodent malaria parasites infect erythroblasts that express major histocompatibility complex (MHC) class I antigens, which are recognized by CD8(+) T cells. In this study, we demonstrate that the cytotoxic activity of CD8(+) T cells contributes to the protection of mice against blood-stage malaria in a Fas ligand (FasL)-dependent manner. Erythroblasts infected with malarial parasites express the death receptor Fas. CD8(+) T cells induce the externalization of phosphatidylserine (PS) on the infected erythroblasts in a cell-to-cell contact-dependent manner. PS enhances the engulfment of the infected erythroid cells by phagocytes. As a PS receptor, T-cell immunoglobulin-domain and mucin-domain-containing molecule 4 (Tim-4) contributes to the phagocytosis of malaria-parasite-infected cells. Our findings provide insight into the molecular mechanisms underlying the protective immunity exerted by CD8(+) T cells in collaboration with phagocytes.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4366679PMC
http://dx.doi.org/10.7554/eLife.04232DOI Listing

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