Neospora caninum: Adoptive transfer of immune lymphocytes precipitates disease in BALB/c mice

Spencer, Jennifer; Higginbotham, Michael J.; Young-White, R.R.; Guarino, A. J.; Blagburn, Byron L.

doi:10.1016/j.vetimm.2005.04.001

Cited by 2 publications

(3 citation statements)

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“…These cells have been extensively studied in the context of protozoan infections 15 including those caused by the N. caninum closely related pathogen Toxoplasma gondii 13 29 30 31 . However, the role of CD8 + T cells in the course of neosporosis has only been addressed in a few studies 9 10 14 32 33 . Here, we show that mice lacking CD8 + T cells are more susceptible to N. caninum infection than their WT counterparts during the acute phase of infection.…”

Section: Discussionmentioning

confidence: 99%

“…The lack of complete protection observed in the ScCr mice receiving CD8 + T cells may reflect the need of IL-12-dependent CD4 + T cell or NK cell activation, previously shown to be important in mice infected with the related parasite T. gondii 34 35 . A previous study reported that adoptive transfer of in vivo N. caninum -primed CD8 + T cells prior to infection precipitated neurological disease in resistant BALB/c mice challenged with NcT 14 . The immunocompetent status of these recipients might have contributed to the reported effect, a likely consequence of immunopathology.…”

Section: Discussionmentioning

confidence: 99%

“…Nevertheless, the underlying mechanisms responsible for this protection remain poorly defined. Moreover, another study indicated that these cells could also exacerbate the neurologic symptoms resulting from N. caninum infection 14 . Therefore, a reassessment of the role that these cells may play in N. caninum infection is needed.…”

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confidence: 99%

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Predominant role of interferon-γ in the host protective effect of CD8+ T cells against Neospora caninum infection

Correia

Ferreirinha

Botelho

et al. 2015

Sci Rep

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It is well established that CD8+ T cells play an important role in protective immunity against protozoan infections. However, their role in the course of Neospora caninum infection has not been fully elucidated. Here we report that CD8-deficient mice infected with N. caninum presented higher parasitic loads in the brain and lungs and lower spleen and brain immunity-related GTPases than their wild-type counterparts. Moreover, adoptive transfer of splenic CD8+ T cells sorted from N. caninum-primed immunosufficient C57BL/10 ScSn mice prolonged the survival of infected IL-12-unresponsive C57BL/10 ScCr recipients. In both C57BL/6 and C57BL/10 ScSn mice CD8+ T cells are activated and produce interferon-γ (IFN-γ) upon challenged with N. caninum. The host protective role of IFN-γ produced by CD8+ T cells was confirmed in N. caninum-infected RAG2-deficient mice reconstituted with CD8+ T cells obtained from either IFN-γ-deficient or wild-type donors. Mice receiving IFN-γ-expressing CD8+ T cells presented lower parasitic burdens than counterparts having IFN-γ-deficient CD8+ T cells. Moreover, we observed that N. caninum-infected perforin-deficient mice presented parasitic burdens similar to those of infected wild-type controls. Altogether these results demonstrate that production of IFN-γ is a predominant protective mechanism conferred by CD8+ T cells in the course of neosporosis.

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