Abstract
Cross‐presentation of malaria antigen by brain microvessels: why <scp>CD</scp>8<sup>+</sup> T cells are critical for the pathogenesis of experimental cerebral malaria
Highlights
Cross‐presentation of malaria antigen by brain microvessels: why CD8þ T cells are critical for the pathogenesis of experimental cerebral malaria
Pathogenesis of Cerebral malaria (CM) was previously thought to derive from the occlusion of brain microvessels induced by the sequestration of infected Red blood cells (RBCs), but recent studies show that the etiology of CM is more complex and involves host immune responses
This study indicates that activation of Plasmodium‐specific CD8þ T cells by
Summary
Pathogenesis of CM was previously thought to derive from the occlusion of brain microvessels induced by the sequestration of infected RBCs, but recent studies show that the etiology of CM is more complex and involves host immune responses (de Souza et al, 2010). T cells in the infected mice recognize this PbGAP50 This epitope was expressed in non‐ECM inducing malaria parasites. This study indicates that activation of Plasmodium‐specific CD8þ T cells by DCs in periphery is not directly linked to ECM, and cross‐presentation of malaria antigens by microvessel target cells, is critical for the pathogenesis. Multiple CD8 epitopes are involved in the pathogenesis of ECM, and it would be interesting to find other PbA antigens recognized by CD8þ T cells and ask whether their sum can induce an ECM‐. This study is a significant advance for the understanding of the pathogenesis of ECM, but it seems that the whole picture of ECM pathogenesis is yet to be determined
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