%0 Journal Article
%T Roles of IFN-¦Ã and ¦Ã¦Ä T Cells in Protective Immunity Against Blood-Stage Malaria
%A Shin-Ichi Inoue
%A Fumie Kobayashi
%J Frontiers in Immunology
%D 2013
%I Frontiers Media
%R 10.3389/fimmu.2013.00258
%X Malaria is caused by infection with Plasmodium parasites. Various studies with knockout mice have indicated that IFN-¦Ã plays essential roles in protective immunity against blood-stage Plasmodium infection. However, after Plasmodium infection, increased IFN-¦Ã production by various types of cells is involved not only in protective immunity, but also in immunopathology. Recent reports have shown that IFN-¦Ã acts as a pro-inflammatory cytokine to induce not only the activation of macrophages, but also the generation of uncommon myelolymphoid progenitor cells after Plasmodium infection. However, the effects of IFN-¦Ã on hematopoietic stem cells and progenitor cells are unclear. Therefore, the regulation of hematopoiesis by IFN-¦Ã during Plasmodium infection remains to be clarified. Although there are conflicting reports concerning the significance of ¦Ã¦Ä T cells in protective immunity against Plasmodium infection, ¦Ã¦Ä T cells may respond to infection and produce IFN-¦Ã as innate immune cells in the early phase of blood-stage malaria. Our recent studies have shown that ¦Ã¦Ä T cells express CD40 ligand and produce IFN-¦Ã after Plasmodium infection, resulting in the enhancement of dendritic cell activation as part of the immune response to eliminate Plasmodium parasites. These data suggest that the function of ¦Ã¦Ä T cells is similar to that of NK cells. Although several reports suggest that ¦Ã¦Ä T cells have the potential to act as memory cells for various infections, it remains to be determined whether memory ¦Ã¦Ä T cells are generated by Plasmodium infection and whether memory ¦Ã¦Ä T cells can contribute to the host defense against re-infection with Plasmodium. Here, we summarize and discuss the effects of IFN-¦Ã and the various functions of ¦Ã¦Ä T cells in blood-stage Plasmodium infection.
%K IFN-¦Ã
%K ¦Ã¦Ä T cells
%K malaria
%K dendritic cells
%K ¦Á¦Â T cells
%K memory cells
%K hematopoiesis
%U http://www.frontiersin.org/Journal/10.3389/fimmu.2013.00258/abstract