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dc.contributor.authorRekdal, Ø.
dc.contributor.authorEspevik, T.
dc.contributor.authorKonopski, Z.
dc.contributor.authorSvendsen, J. S.
dc.contributor.authorWinberg, J.-O.
dc.contributor.authorØsterud, B.
dc.date.accessioned2009-01-07T13:00:40Z
dc.date.available2009-01-07T13:00:40Z
dc.date.issued1994
dc.description.abstractThe present study was performed to examine whether residues 36–62 of TNFα contain the chemotactic domain of TNFα, and whether the p55 and p75 TNF receptors are involved in TNFα induced chemotaxis. The chemotactic effect of TNFα on PMN was inhibited by the mAbs Hrt-7b and Utr-1, against the p55 and p75 TNF receptors, respectively. Both receptors may therefore be required for mediating the chemotactic effect of TNFcz. The synthetic TNFα 36–62, similar to TNFα, had chemotactic effects on both PMN and monocytes. The chemotactic activity of the TNFα 36–62 peptide on PMN, was inhibited by Htr-7b, Utr-1 and soluble p55 receptor, which shows that the peptide possessed the ability to induce chemotaxis through the TNF receptors. In contrast to TNFα, the peptide did not show a cytotoxic activity against WEHI 164 flbrosarcoma cells. It is suggested that different domains of the TNFα molecule induce distinct biological effects.en
dc.format.extent1126607 bytes
dc.format.mimetypeapplication/pdf
dc.identifier.citationMediators of Inflammation, vol. 3, no. 5, pp. 347-352, 1994. doi:10.1155/S0962935194000487en
dc.identifier.urihttps://hdl.handle.net/10037/1703
dc.identifier.urnURN:NBN:no-uit_munin_1440
dc.language.isoengen
dc.publisherHindawi Publishing Corporationen
dc.rights.accessRightsopenAccess
dc.subjectChemotaxisen
dc.subjectMolecular modellingen
dc.subjectSynthetic peptideen
dc.subjectTNFαen
dc.subjectTNF receptorsen
dc.subjectVDP::Mathematics and natural science: 400::Basic biosciences: 470::General microbiology: 472en
dc.titleThe TNF Receptors p55 and p75 Mediate Chemotaxis of PMN Induced by TNFα and a TNFα 36–62 Peptideen
dc.typeJournal articleen
dc.typeTidsskriftartikkelen
dc.typePeer revieweden


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