Abstract
Using tumor necrosis factor receptor type 2 (TNFR2)-deficient mice and generating bone marrow chimeras which express TNFR2 on either hematopoietic or nonhematopoietic cells, we demonstrated the requirement for TNFR2 expression on tissue cells to induce lethal cerebral malaria. Thus, TNFR2 on the brain vasculature mediates tumor necrosis factor-induced neurovascular lesions in experimental cerebral malaria.
MeSH terms
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Animals
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Antigens, CD / genetics
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Antigens, CD / physiology*
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Blood Platelets / pathology
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Blood Vessels / immunology*
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Bone Marrow Transplantation
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Cerebrovascular Circulation / immunology
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Chimera
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Endothelium, Vascular / immunology
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Malaria, Cerebral / etiology*
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Malaria, Cerebral / immunology
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Malaria, Cerebral / pathology
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Mice
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Mice, Inbred C57BL
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Mice, Knockout
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Parasitemia / etiology
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Parasitemia / immunology
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Plasmodium berghei*
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Receptors, Tumor Necrosis Factor / deficiency
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Receptors, Tumor Necrosis Factor / genetics
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Receptors, Tumor Necrosis Factor / physiology*
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Receptors, Tumor Necrosis Factor, Type II
Substances
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Antigens, CD
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Receptors, Tumor Necrosis Factor
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Receptors, Tumor Necrosis Factor, Type II