title: CD4+ T cells are required for HSP65 expression in host macrophages and for protection of mice infected with Plasmodium yoelii.
abstract: We have reported that macrophages expressing heat-shock protein 65 play an essential role in protection of mice infected with Plasmodium yoelii. In this study, we investigated the function and expression mechanism of HSP65 in macrophages of mice infected with P. yoelii. C57BL/6 (B6) mice are susceptible to infection with the lethal (L) strain but resistant to infection with the non-lethal (NL) strain of P. yoelii. The percentage of apoptotic macrophages in mice infected with the L strain was higher than that in mice infected with the NL strain. However, the percentage was low in L strain infected mice if they acquired resistance to the infection by primary infection with the NL strain. That apoptosis was reversely correlated with HSP65 expression in splenic macrophages from mice infected with P. yoelii suggests HSP65 may contribute to protective immunity by preventing apoptosis of macrophages in malarial infection. Cell depletion/transfer experiments showed that CD4+ T cells, but not CD8+ T cells, gammadelta T cells, NK cells or NK T cells, were required for HSP65 expression in macrophages as well as for protection of mice infected with P. yoelii. In conclusion, HSP65 may play a role in preventing apoptosis of macrophages in mice infected with P. yoelii. CD4+ T cells are required for HSP65 expression and for protective immunity against P. yoelii infection.
authors.affiliation: Department of Parasitology and Immunology, The University of Tokushima, School of Medicine, Tokushima, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Zhang
authors.forename: H
authors.initials: H
authors.lastname: Hisaeda
authors.forename: T
authors.initials: T
authors.lastname: Sakai
authors.forename: Y
authors.initials: Y
authors.lastname: Li
authors.forename: H
authors.initials: H
authors.lastname: Ishikawa
authors.forename: Y P
authors.initials: YP
authors.lastname: Hao
authors.forename: Y
authors.initials: Y
authors.lastname: Nakano
authors.forename: Y
authors.initials: Y
authors.lastname: Ito
authors.forename: K
authors.initials: K
authors.lastname: Himeno
mesh_terms: D000818:Animals; D017209:Apoptosis; D015153:Blotting, Western; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D005260:Female; D006360:Heat-Shock Proteins / Q000378:metabolism*; D008212:Lymphocyte Depletion; D008264:Macrophages / Q000276:immunology / Q000378:metabolism* / Q000469:parasitology; D008288:Malaria / Q000276:immunology* / Q000469:parasitology; D051379:Mice; D008810:Mice, Inbred C57BL; D008819:Mice, Nude; D016513:Mice, SCID; D018512:Parasitemia / Q000276:immunology / Q000469:parasitology; D010967:Plasmodium yoelii / Q000276:immunology; D014774:Virulence
chemical_list: D006360:Heat-Shock Proteins