@article{oai:nagasaki-u.repo.nii.ac.jp:00006135,
 author = {Bao, Lam Quoc and Huy, Nguyen Tien and Kikuchi, Mihoko and Yanagi, Tetsuo and Senba, Masachika and Shuaibu, Mohammed Nasir and Honma, Kiri and Yui, Katsuyuki and Hirayama, Kenji},
 issue = {5},
 journal = {PLoS ONE},
 month = {May},
 note = {In African endemic area, adults are less vulnerable to cerebral malaria than children probably because of acquired partial immunity or semi-immune status. Here, we developed an experimental cerebral malaria (ECM) model for semi-immune mice. C57BL/6 (B6) mice underwent one, two and three cycles of infection and radical treatment (1-cure, 2-cure and 3-cure, respectively) before being finally challenged with 104 Plasmodium berghei ANKA without treatment. Our results showed that 100% of naïve (0-cure), 67% of 1-cure, 37% of 2-cure and none of 3-cure mice succumbed to ECM within 10 days post challenge infection. In the protected 3-cure mice, significantly higher levels of plasma IL-10 and lower levels of IFN-γ than the others on day 7 post challenge infection were observed. Major increased lymphocyte subset of IL-10 positive cells in 3-cure mice was CD5(-)CD19(+) B cells. Passive transfer of splenic CD19(+) cells from 3-cure mice protected naïve mice from ECM. Additionally, aged 3-cure mice were also protected from ECM 12 and 20 months after the last challenge infection. In conclusion, mice became completely resistant to ECM after three exposures to malaria. CD19(+) B cells are determinants in protective mechanism of semi-immune mice against ECM possibly via modulatory IL-10 for pathogenic IFN-γ production., PLoS ONE, 8(5), e64836; 2013},
 title = {CD19(+) B Cells Confer Protection against Experimental Cerebral Malaria in Semi-Immune Rodent Model},
 volume = {8},
 year = {2013}
}