title: CD19(+) B cells confer protection against experimental cerebral malaria in semi-immune rodent model.
abstract: 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 10(4) 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.
authors.affiliation: Department of Immunogenetics, Institute of Tropical Medicine, Nagasaki University, Nagasaki, Japan.
authors.forename: Lam Quoc
authors.initials: LQ
authors.lastname: Bao
authors.forename: Nguyen Tien
authors.initials: NT
authors.lastname: Huy
authors.forename: Mihoko
authors.initials: M
authors.lastname: Kikuchi
authors.forename: Tetsuo
authors.initials: T
authors.lastname: Yanagi
authors.forename: Masachika
authors.initials: M
authors.lastname: Senba
authors.forename: Mohammed Nasir
authors.initials: MN
authors.lastname: Shuaibu
authors.forename: Kiri
authors.initials: K
authors.lastname: Honma
authors.forename: Katsuyuki
authors.initials: K
authors.lastname: Yui
authors.forename: Kenji
authors.initials: K
authors.lastname: Hirayama
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D000913:Antibodies, Protozoan / Q000097:blood; D018941:Antigens, CD19 / Q000378:metabolism*; D001402:B-Lymphocytes / Q000276:immunology*; D018956:CD5 Antigens / Q000378:metabolism; D004195:Disease Models, Animal; D060467:Disease Resistance / Q000276:immunology; D004198:Disease Susceptibility; D007074:Immunoglobulin G / Q000097:blood; D007371:Interferon-gamma / Q000097:blood; D016753:Interleukin-10 / Q000096:biosynthesis / Q000097:blood; D016779:Malaria, Cerebral / Q000097:blood / Q000276:immunology* / Q000469:parasitology / Q000517:prevention & control*; D051379:Mice; D008810:Mice, Inbred C57BL; D018512:Parasitemia / Q000276:immunology / Q000469:parasitology; D010962:Plasmodium berghei / Q000502:physiology; D013045:Species Specificity; D013154:Spleen / Q000473:pathology
chemical_list: D000913:Antibodies, Protozoan; D018941:Antigens, CD19; D018956:CD5 Antigens; D007074:Immunoglobulin G; D016753:Interleukin-10; D007371:Interferon-gamma