Role of L3T4+ and Lyt-2+ T cell subsets in protective immune responses of mice against infection with a low or high virulent strain of Toxoplasma gondii.
TLDR
Lyt‐2+ T cells alone appear to be final effector cells for protection against the challenge with high virulent RH strain tachyzoites, since treatment of the bradyzoite‐immune mice with anti‐Lyt‐2 antibody, but not anti-L3T4 antibody, before challenge significantly increased mortality.Abstract:
In order to elucidate the role of T cell subsets in protective immunity against infection with high virulent and low virulent strains of Toxoplasma gondii, monoclonal antibodies specific for T cell subsets were injected into mice before immunization or challenge infection. Treatment of mice with monoclonal antibody to either L3T4+ or Lyt-2+ T cells before they were immunized with Toxoplasma cell homogenate prepared from high virulent RH strain tachyzoites markedly reduced survival after mice were challenged with low virulent bradyzoites of the Beverley strain. Thus, induction of protective immunity against bradyzoites of the Beverley strain requires the presence of both L3T4+ and Lyt-2+ T cells. In contrast, mice injected with living bradyzoites of the low virulent Beverley strain after immunization with Toxoplasma cell homogenate acquired protective immunity against high virulent tachyzoites of the RH strain. Lyt-2+ T cells alone appear to be final effector cells for protection against the challenge with high virulent RH strain tachyzoites, since treatment of the bradyzoite-immune mice with anti-Lyt-2 antibody, but not anti-L3T4 antibody, before challenge significantly increased mortality.read more
Citations
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Journal ArticleDOI
B cells are essential for vaccination-induced resistance to virulent Toxoplasma gondii.
TL;DR: The hypothesis that B cells are required for vaccination-induced resistance to virulent tachyzoites in order to produce antibodies is supported and that antibodies may function protectively in vivo by blocking infection of host cells by tachyzosites.
Journal Article
Immune response to Toxoplasma gondii.
Denis Filisetti,Ermanno Candolfi +1 more
TL;DR: Oral-route infection with Toxoplasma gondii sporozoites or tachyzoites leads to the rapid spread of quick-replicating cytolytic tachyozoites throughout the whole body, aiding the survival of the parasite by converting it into a bradyzoite, an intracellular quiescent resistant form persisting in the muscle and brain tissues.
Journal ArticleDOI
CD4+ Vα14 NKT cells play a crucial role in an early stage of protective immunity against infection with Leishmania major.
Hiroyuki Ishikawa,Hajime Hisaeda,Masaru Taniguchi,Toshinori Nakayama,Tohru Sakai,Yoichi Maekawa,Yoko Nakano,Manxin Zhang,Tianqian Zhang,Masaaki Nishitani,Miwa Takashima,Kunisuke Himeno +11 more
TL;DR: The roles of gamma delta T, NK and NKT cells in an early stage of protective immunity against infection with Leishmania major were investigated and the contribution of these innate cells to the expression of 65 kDa heat shock protein in host macrophages was examined.
Journal ArticleDOI
Deficient Humoral Responses Underlie Susceptibility to Toxoplasma gondii in CD4-Deficient Mice
TL;DR: It is demonstrated that in addition to CD8+ T cells and IFN-γ, which are known to be critical for resistance, CD4+ cells also contribute significantly to protection against chronic T. gondii infections and against challenge infections with highly virulent tachyzoites in immunized mice via their role as helper cells for production of isotype-switched antibodies.
Journal ArticleDOI
Human dendritic cells discriminate between viable and killed Toxoplasma gondii tachyzoites: dendritic cell activation after infection with viable parasites results in CD28 and CD40 ligand signaling that controls IL-12-dependent and -independent T cell production of IFN-gamma.
TL;DR: T. gondii-induced activation of human DC is associated with T cell production of IFN-γ through CD40-CD40L-dependent release of IL-12 and through CD80/CD86-CD28 andCD40- CD40L signaling that mediate IFn-γ secretion even in the absence of bioactive IL- 12.
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TL;DR: There are substantial roles for both the Lyt-2+ and LyT-1+, L3T4 T cell subsets in dual regulation of resistance against toxoplasma infection and that Lyt -2+ T cells are the principal mediator of the resistance.