{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,10]],"date-time":"2026-02-10T08:58:38Z","timestamp":1770713918214,"version":"3.49.0"},"reference-count":29,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2005,11,23]],"date-time":"2005-11-23T00:00:00Z","timestamp":1132704000000},"content-version":"vor","delay-in-days":3067,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[1997,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Tumor necrosis factor (TNF) has been implicated in the pathogenesis of experimental cerebral malaria (CM), but the respective role of its two types of receptors has not been established. A significant increase in the expression of TNF\u2010receptor 2 (TNFR2, p75), but not of TNFR1 (p55), was found on brain microvessels at the time of CM in susceptible animals. Moreover, mice genetically deficient for TNFR2 (<jats:italic>Tnfr2<\/jats:italic>\u00b0) were significantly protected from experimental CM, in contrast to TNFR1\u2010deficient (<jats:italic>Tnfr1<\/jats:italic>\u00b0) mice, which were as susceptible as wild\u2010type mice. To identify the factors involved in the protection from CM conferred by the lack of TNFR2, we assessed in both knockout and control mice the serum concentrations of mediators that are critical for the development of CM, as well as the up\u2010regulation of intercellular adhesion molecule\u20101 (ICAM\u20101) in the brain microvessels. No significant difference in serum levels of TNF and interferon\u2010\u03b3 was found between infected wild\u2010type and <jats:italic>Tnfr1<\/jats:italic>\u00b0 or <jats:italic>Tnfr2<\/jats:italic>\u00b0 mice. Interestingly, the pronounced ICAM\u20101 up\u2010regulation and leukocyte sequestration, typically occurring in brain microvessels of CM\u2010susceptible animals, was detected in infected control and <jats:italic>Tnfr1<\/jats:italic>\u00b0 mice \u2013 both of which developed CM \u2013 whereas no such ICAM\u20101 up\u2010regulation or leukocyte sequestration was observed in <jats:italic>Tnfr2<\/jats:italic>\u00b0 mice, which were protected from CM. Making use of microvascular endothelium cells (MVEC) isolated from wild\u2010type, <jats:italic>Tnfr1<\/jats:italic>\u00b0 or <jats:italic>Tnfr2<\/jats:italic>\u00b0 mice, we show that soluble TNF requires the presence of both TNF receptors, whereas membrane\u2010bound TNF only needs TNFR2 for TNF\u2010mediated ICAM\u20101 up\u2010regulation in brain MVEC. Thus, only in MVEC lacking TNFR2, neither membrane\u2010bound nor soluble TNF cause the up\u2010regulation of ICAM\u20101 <jats:italic>in vitro.<\/jats:italic> In conclusion, these results indicate that the interaction between membrane TNF and TNFR2 is crucial in the development of this neurological syndrome.<\/jats:p>","DOI":"10.1002\/eji.1830270719","type":"journal-article","created":{"date-parts":[[2007,3,2]],"date-time":"2007-03-02T05:21:40Z","timestamp":1172812900000},"page":"1719-1725","source":"Crossref","is-referenced-by-count":124,"title":["Crucial role of tumor necrosis factor (TNF) receptor 2 and membrane\u2010bound TNF in experimental cerebral malaria"],"prefix":"10.1002","volume":"27","author":[{"given":"Rudolf","family":"Lucas","sequence":"first","affiliation":[]},{"given":"Pierre","family":"Juillard","sequence":"additional","affiliation":[]},{"given":"Els","family":"Decoster","sequence":"additional","affiliation":[]},{"given":"Mireille","family":"Redard","sequence":"additional","affiliation":[]},{"given":"Danielle","family":"Burger","sequence":"additional","affiliation":[]},{"given":"Yves","family":"Donati","sequence":"additional","affiliation":[]},{"given":"Christine","family":"Giroud","sequence":"additional","affiliation":[]},{"given":"Christine","family":"Monso\u2010Hinard","sequence":"additional","affiliation":[]},{"given":"Toon","family":"De Kesel","sequence":"additional","affiliation":[]},{"given":"Wim A.","family":"Buurman","sequence":"additional","affiliation":[]},{"given":"Mark W.","family":"Moore","sequence":"additional","affiliation":[]},{"given":"Jean\u2010Michel","family":"Dayer","sequence":"additional","affiliation":[]},{"given":"Walter","family":"Fiers","sequence":"additional","affiliation":[]},{"given":"Horst","family":"Bluethmann","sequence":"additional","affiliation":[]},{"given":"Georges E.","family":"Grau","sequence":"additional","affiliation":[]}],"member":"311","published-online":{"date-parts":[[2005,11,23]]},"reference":[{"key":"e_1_2_1_2_2","doi-asserted-by":"crossref","first-page":"2348","DOI":"10.4049\/jimmunol.137.7.2348","volume":"137","author":"Grau G. 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