Abstract
The respective role of the two receptors of TNF in experimental cerebral malaria (CM) was investigated. During CM, a significant upregulation of TNF-receptor 2 (TNFR2), but not of TNFR1, was found in brain microvessels of susceptible, but not resistant mice. Mice genetically deficient for TNFR2 (Tnfr2°) were significantly protected from CM, while TNFR1-deficient (Tfnr1°) mice were as susceptible as wild-type mice. The protection of Tnfr2° mice could be explained by their absence of ICAM-1 upregulation and leukocyte sequestration, known to occur in brain microvessels of CM-susceptible animals.
Original language | English (US) |
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Pages (from-to) | 143-148 |
Number of pages | 6 |
Journal | Journal of Neuroimmunology |
Volume | 72 |
Issue number | 2 |
DOIs | |
State | Published - Feb 1997 |
Externally published | Yes |
Keywords
- ICAM-1
- Plasmodium berghei
- TNF receptor 2
- cerebral malaria
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Neurology
- Clinical Neurology