title: Involvement of CD8+ T cells in protective immunity against murine blood-stage infection with Plasmodium yoelii 17XL strain.
abstract: When developing malaria vaccines, the most crucial step is to elucidate the mechanisms involved in protective immunity against the parasites. We found that CD8(+) T cells contribute to protective immunity against infection with blood-stage parasites of Plasmodium yoelii. Infection of C57BL/6 mice with P. yoelii 17XL was lethal, while all mice infected with a low-virulence strain of the parasite 17XNL acquired complete resistance against re-infection with P. yoelii 17XL. However, the host mice transferred with CD8(+) T cells from mice primed only with P. yoelii 17XNL failed to acquire protective immunity. On the other hand, the irradiated host mice were completely resistant to P. yoelii 17XL infection, showing no grade of parasitemia when adoptively transferred with CD8(+) T cells from immune mice that survived infection with both P. yoelii XNL and, subsequently, P. yoelii 17XL. These protective CD8(+) T cells from immune WT mice had the potential to generate IFN-gamma, perforin (PFN) and granzyme B. When mice deficient in IFN-gamma were used as donor mice for CD8(+) T cells, protective immunity in the host mice was fully abrogated, and the immunity was profoundly attenuated in PFN-deficient mice. Thus, CD8(+) T cells producing IFN-gamma and PFN appear to be involved in protective immunity against infection with blood-stage malaria.
authors.affiliation: Department of Microbiology and Immunology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan. t-imai@rcai.riken.jp
authors.forename: Takashi
authors.initials: T
authors.lastname: Imai
authors.forename: Jianying
authors.initials: J
authors.lastname: Shen
authors.forename: Bin
authors.initials: B
authors.lastname: Chou
authors.forename: Xuefeng
authors.initials: X
authors.lastname: Duan
authors.forename: Liping
authors.initials: L
authors.lastname: Tu
authors.forename: Kohhei
authors.initials: K
authors.lastname: Tetsutani
authors.forename: Chikako
authors.initials: C
authors.lastname: Moriya
authors.forename: Hidekazu
authors.initials: H
authors.lastname: Ishida
authors.forename: Shinjiro
authors.initials: S
authors.lastname: Hamano
authors.forename: Chikako
authors.initials: C
authors.lastname: Shimokawa
authors.forename: Hajime
authors.initials: H
authors.lastname: Hisaeda
authors.forename: Kunisuke
authors.initials: K
authors.lastname: Himeno
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology* / Q000378:metabolism / Q000637:transplantation; D003289:Convalescence; D004268:DNA-Binding Proteins / Q000172:deficiency / Q000235:genetics; D005260:Female; D053804:Granzymes / Q000096:biosynthesis; D007371:Interferon-gamma / Q000096:biosynthesis / Q000172:deficiency / Q000235:genetics; D008264:Macrophages / Q000276:immunology; D008288:Malaria / Q000276:immunology* / Q000517:prevention & control; D017780:Malaria Vaccines / Q000276:immunology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D018512:Parasitemia / Q000276:immunology* / Q000517:prevention & control; D010967:Plasmodium yoelii / Q000276:immunology* / Q000472:pathogenicity; D052899:Pore Forming Cytotoxic Proteins / Q000096:biosynthesis / Q000172:deficiency / Q000235:genetics; D011828:Radiation Chimera; D014774:Virulence
chemical_list: D004268:DNA-Binding Proteins; D017780:Malaria Vaccines; D052899:Pore Forming Cytotoxic Proteins; C499308:Rag2 protein, mouse; C483886:perforin, mouse; D007371:Interferon-gamma; D053804:Granzymes; C509214:Gzmb protein, mouse