title: Reasons why DBA/2 mice are resistant to malarial infection: expansion of CD3int B220+ gammadelta T cells with double-negative CD4- CD8- phenotype in the liver.
abstract: DBA/2 (H-2(d)) mice are known to be more resistant than C57BL/6 (B6, H-2(b)) mice to the non-lethal 17XNL strain of Plasmodium yoelii. This is a very strange phenomenon because the functions of conventional T cells, especially CD8(+) T cells, are known to be somewhat lower in DBA/2 mice than in other strains of mice. We examined herein how immune responses differed between DBA/2 mice and B6 mice during malarial infection. DBA/2 mice and (DBA/2 x B6)F(1) (BDF(1), H-2(b/d)) mice were found to have milder parasitaemia and to recover more quickly from malarial infection than B6 mice. These DBA/2 and BDF(1) mice were also found to experience a marked expansion of interleukin (IL)-2Rbeta(+) CD3(int) cells and gammadelta T cells in the liver, especially in the recovery phase. The expansion of unconventional T cells (i.e. B220(+) T cells) was also marked in DBA/2 and BDF(1) mice. The majority of B220(+) T cells were gammadelta T cells and these T cells were double-negative CD4(-) CD8(-). More importantly, the production of immunoglobulin M (IgM)-type anti-DNA autoantibody was also higher in DBA/2 and BDF(1) mice than in B6 mice. In conjunction with data on cytokine production, these results indicate that primitive T and B cells, namely autoreactive extrathymic T cells and autoantibody-producing B cells, may be much more activated in DBA/2 mice and therefore resistant to the non-lethal 17XNL strain of P. yoelii.
authors.affiliation: Department of Immunology, Niigata University School of Medicine, Niigata, Japan.
authors.forename: Hanaa Y
authors.initials: HY
authors.lastname: Bakir
authors.forename: Chikako
authors.initials: C
authors.lastname: Tomiyama-Miyaji
authors.forename: Hisami
authors.initials: H
authors.lastname: Watanabe
authors.forename: Toru
authors.initials: T
authors.lastname: Nagura
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Kawamura
authors.forename: Hiroho
authors.initials: H
authors.lastname: Sekikawa
authors.forename: Toru
authors.initials: T
authors.lastname: Abo
mesh_terms: D000818:Animals; D000974:Antibodies, Antinuclear / Q000096:biosynthesis; D000911:Antibodies, Monoclonal / Q000276:immunology; D017252:CD3 Complex / Q000032:analysis; D016207:Cytokines / Q000096:biosynthesis; D007113:Immunity, Innate; D007075:Immunoglobulin M / Q000096:biosynthesis; D016130:Immunophenotyping; D017493:Leukocyte Common Antigens / Q000032:analysis; D008099:Liver / Q000276:immunology*; D008288:Malaria / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D008811:Mice, Inbred DBA; D018512:Parasitemia / Q000276:immunology; D010967:Plasmodium yoelii; D016692:Receptors, Antigen, T-Cell, gamma-delta / Q000032:analysis / Q000276:immunology; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D013154:Spleen / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000276:immunology*
chemical_list: D000974:Antibodies, Antinuclear; D000911:Antibodies, Monoclonal; D017252:CD3 Complex; D016207:Cytokines; D007075:Immunoglobulin M; D016692:Receptors, Antigen, T-Cell, gamma-delta; D017493:Leukocyte Common Antigens