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Malaria protection in β 2 ‐microglobulin‐deficient mice lacking major histocompatibility complex class I antigens: essential role of innate immunity, including γδT cells
Author(s) -
Taniguchi Tomoyo,
Tachikawa Saoko,
Kanda Yasuhiro,
Kawamura Toshihiko,
TomiyamaMiyaji Chikako,
Li Changchun,
Watanabe Hisami,
Sekikawa Hiroho,
Abo Toru
Publication year - 2007
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2007.02661.x
Subject(s) - immunology , biology , natural killer t cell , immunity , innate immune system , cd8 , plasmodium yoelii , major histocompatibility complex , cytotoxic t cell , antigen , immune system , malaria , parasitemia , plasmodium falciparum , genetics , in vitro
Summary It is still controversial whether malaria protection is mediated by conventional immunity associated with T and B cells or by innate immunity associated with extrathymic T cells and autoantibody‐producing B cells. Given this situation, it is important to examine the mechanism of malaria protection in β 2 ‐microglobulin‐deficient (β 2 m(–/–)) mice. These mice lack major histocompatibility complex class I and CD1d antigens, which results in the absence of CD8 + T cells and natural killer T (NKT) cells. When C57BL/6 and β 2 m(–/–) mice were injected with parasitized ( Plasmodium yoelii 17XNL) erythrocytes, both survived from the infection and showed a similar level of parasitaemia. The major expanding T cells were NK1.1 – αβΤ‐cell receptor int cells in both mice. The difference was a compensatory expansion of NK and γδT cells in β 2 m(–/–) mice, and an elimination experiment showed that these lymphocytes were critical for protection in these mice. These results suggest that malaria protection might be events of the innate immunity associated with multiple subsets with autoreactivity. CD8 + T and NKT cells may be partially related to this protection.