TY - JOUR
T1 - Cutting edge: Dendritic cells are essential for in vivo IL-12 production and development of resistance against Toxoplasma gondii infection in mice
AU - Minor, Radiah
AU - Liu, Cheng Hu
AU - Fan, Yu Ting
AU - Dias, Alexandra
AU - Esper, Lisia
AU - Corn, Radiah A.
AU - Bafica, Andre
AU - Machado, Fabiana S.
AU - Aliberti, Julio
PY - 2006
Y1 - 2006
N2 - A powerful IFN-γ response is triggered upon infection with the protozoan parasite, Toxoplasma gondii. Several cell populations, including dendritic cells (DCs), macrophages, and neutrophih, produce IL-12, a key cytokine for IFN-γ induction. However, it is still unclear which of the above cell populations is its main source. Diphtheria toxin (DT) injection causes transient DC depletion in a transgenic mouse expressing Simian DT receptors under the control of the CD11c promoter, allowing us to investigate the role of DCs in IL-12 production. T. gondii-inoculated DT-treated and control groups were monitored for IL-12 levels and survival. We show in this study that DC depletion abolished IL-12 production and led to mortality. Furthermore, replenishment with wild-type, but not MyD88- or IL-12p35-deficient, DCs rescued IL-12 production, IFN-γ-induction, and resistance to infection in DC-depleted mice. Taken together, the results presented in this study indicate that DCs constitute the major IL-12-producing cell population in vivo during T. gondii infection. Copyright © 2006 by The American Association of Immunologists, Inc.
AB - A powerful IFN-γ response is triggered upon infection with the protozoan parasite, Toxoplasma gondii. Several cell populations, including dendritic cells (DCs), macrophages, and neutrophih, produce IL-12, a key cytokine for IFN-γ induction. However, it is still unclear which of the above cell populations is its main source. Diphtheria toxin (DT) injection causes transient DC depletion in a transgenic mouse expressing Simian DT receptors under the control of the CD11c promoter, allowing us to investigate the role of DCs in IL-12 production. T. gondii-inoculated DT-treated and control groups were monitored for IL-12 levels and survival. We show in this study that DC depletion abolished IL-12 production and led to mortality. Furthermore, replenishment with wild-type, but not MyD88- or IL-12p35-deficient, DCs rescued IL-12 production, IFN-γ-induction, and resistance to infection in DC-depleted mice. Taken together, the results presented in this study indicate that DCs constitute the major IL-12-producing cell population in vivo during T. gondii infection. Copyright © 2006 by The American Association of Immunologists, Inc.
UR - https://dx.doi.org/10.4049/jimmunol.177.1.31
U2 - 10.4049/jimmunol.177.1.31
DO - 10.4049/jimmunol.177.1.31
M3 - Article
VL - 177
JO - Journal of Immunology
JF - Journal of Immunology
IS - Issue 1
ER -