Anemia 2013 July-1


CD8+ T cell activation by murine erythroblasts infected with malaria parasites

Sci Rep. 2013;3:1572.

Takashi Imai1, Hidekazu Ishida2, Kazutomo Suzue1, Makoto Hirai1, Tomoyo Taniguchi1, 3, Hiroko Okada1, Tomohisa Suzuki1, Chikako Shimokawa4, and Hajime Hisaeda1


1Department of Parasitology, Graduate School of Medicine, Gunma University, Gunma 371-8511, Japan

2Department of Microbiology and Immunology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan

3Center for Medical Education, Faculty of Medicine, Gunma University, Gunma 371-8511, Japan

4Department of Parasitology, Institute of Tropical Medicine, Nagasaki University, Nagasaki 852-8523, Japan



Malaria is considered one of the world’s biggest three infectious diseases along with AIDS and tuberculosis. Understanding host immune responses against malaria parasite and their life cycle in detail is important for vaccine development. Recently, studies have shown that human malaria parasites parasitize erythroblasts, though whose significance is unclear. Here, we tried to clarify its biological importance using a murine model. It is confirmed that erythroblasts were parasitized in the bone marrow and spleen, which is the first report for mouse erythroblasts parasitized by malaria parasites. Furthermore, parasitized erythroblasts were found a potential source of new infection, indicating that erythroblast parasitism is a part of life cycle of the parasites. In addition, immunological importance of erythroblast parasitism is also revealed. Our previous report demonstrated protective roles of CD8+ T cells against blood-stage malaria partially attributed to their cytotoxic activities, suggesting cytotoxicity towards MHC class I-expressing erythroblast in contrast to erythrocytes lacking MHC class I. Indeed, parasitized erythroblasts were recognized by CD8+ T cells in an antigen-specific manner, followed by production of IFN-g from those cells.  Our findings provide a new insight into host-parasite relationship during malaria, which supports development malaria vaccines that activate CD8+ T cells.

PMID: 23535896

Takashi Imai-1

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