Sarcocystis neurona is an apicomplexan parasite that is the primary etiologic agent of equine protozoal myeloencephalitis in horses. Protective immune responses in horses have not been determined, but interferon-γ (IFN-γ) is considered critical for protection from neurologic disease in mice. The role of adaptive and innate immune responses in control of parasites was explored by infecting BALB/c, IFN-γ knockout (GKO), and severe combined immune deficient (SCID) mice with S. neurona (104 sporocysts/mouse). Immune competent BALB/c mice eliminated parasites within 30 days, with no sign of neurologic disease, whereas GKO mice developed fulminant neurologic disease. In contrast, SCID mice remained healthy throughout the experimental period despite the persistence of parasite at low levels in some mice. Treatment with anti–IFN-γ antibody resulted in neurologic disease in infected SCID mice. Although SCID mice lack adaptive immune responses, they have natural killer (NK) cells capable of producing significant quantities of IFN-γ. Therefore, SCID mice were infected with sporocysts of S. neurona and treated with anti-asialo GM1. Depletion of NK cells, confirmed by flow cytometry, did not result in neurologic disease in SCID mice. These results indicate that IFN-γ mediates protection from neurologic disease in SCID mice. Protective levels of IFN-γ may originate from a low number of nondepleted NK cells or from a non-T cell, non-NK cell population.
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August 2004
PATHOLOGY|
August 01 2004
DEPLETION OF NATURAL KILLER CELLS DOES NOT RESULT IN NEUROLOGIC DISEASE DUE TO SARCOCYSTIS NEURONA IN MICE WITH SEVERE COMBINED IMMUNODEFICIENCY
Debra C. Sellon;
Debra C. Sellon
Department of Veterinary Clinical Sciences, Washington State University, Pullman, Washington 99164. [email protected]
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Donald P. Knowles;
Donald P. Knowles
Department of Veterinary Clinical Sciences, Washington State University, Pullman, Washington 99164. [email protected]
* Animal Disease Research Unit, ARS-USDA, Pullman, Washington 99164
† Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, Washington 99164
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Ellis C. Greiner;
Ellis C. Greiner
Department of Veterinary Clinical Sciences, Washington State University, Pullman, Washington 99164. [email protected]
‡ Department of Pathobiology, University of Florida, Gainesville, Florida 32611
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Maureen T. Long;
Maureen T. Long
Department of Veterinary Clinical Sciences, Washington State University, Pullman, Washington 99164. [email protected]
§ Department of Large Animal Clinical Sciences, University of Florida, Gainesville, Florida 32611
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Melissa T. Hines;
Melissa T. Hines
Department of Veterinary Clinical Sciences, Washington State University, Pullman, Washington 99164. [email protected]
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Tressa Hochstatter;
Tressa Hochstatter
Department of Veterinary Clinical Sciences, Washington State University, Pullman, Washington 99164. [email protected]
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Kristin M. Hasel;
Kristin M. Hasel
Department of Veterinary Clinical Sciences, Washington State University, Pullman, Washington 99164. [email protected]
† Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, Washington 99164
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Massaro Ueti;
Massaro Ueti
Department of Veterinary Clinical Sciences, Washington State University, Pullman, Washington 99164. [email protected]
† Department of Veterinary Microbiology and Pathology, Washington State University, Pullman, Washington 99164
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Karen Gillis;
Karen Gillis
Department of Veterinary Clinical Sciences, Washington State University, Pullman, Washington 99164. [email protected]
§ Department of Large Animal Clinical Sciences, University of Florida, Gainesville, Florida 32611
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John B. Dame
John B. Dame
Department of Veterinary Clinical Sciences, Washington State University, Pullman, Washington 99164. [email protected]
‡ Department of Pathobiology, University of Florida, Gainesville, Florida 32611
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J Parasitol (2004) 90 (4): 782–788.
Citation
Debra C. Sellon, Donald P. Knowles, Ellis C. Greiner, Maureen T. Long, Melissa T. Hines, Tressa Hochstatter, Kristin M. Hasel, Massaro Ueti, Karen Gillis, John B. Dame; DEPLETION OF NATURAL KILLER CELLS DOES NOT RESULT IN NEUROLOGIC DISEASE DUE TO SARCOCYSTIS NEURONA IN MICE WITH SEVERE COMBINED IMMUNODEFICIENCY. J Parasitol 1 August 2004; 90 (4): 782–788. doi: https://doi.org/10.1645/GE-205R
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