The TNF Receptors p55 and p75 Mediate Chemotaxis of PMN Induced byTNFα and a TNFα 36–62 Peptide

[摘要] The present study was performed to examine whether residues36–62 of TNFα contain the chemotactic domain ofTNFα, and whether the p55 and p75 TNF receptors are involvedin TNFα induced chemotaxis. The chemotactic effect ofTNFα on PMN was inhibited by the mAbs Hrt-7b and Utr-1,against the p55 and p75 TNF receptors, respectively. Both receptors maytherefore be required for mediating the chemotactic effect of TNFcz.The synthetic TNFα 36–62, similar to TNFα, hadchemotactic effects on both PMN and monocytes. The chemotacticactivity of the TNFα 36–62 peptide on PMN, was inhibitedby Htr-7b, Utr-1 and soluble p55 receptor, which shows that thepeptide possessed the ability to induce chemotaxis through the TNFreceptors. In contrast to TNFα, the peptide did not show acytotoxic activity against WEHI 164 flbrosarcoma cells. It issuggested that different domains of the TNFα molecule inducedistinct biological effects.

[学科分类] 生理学与病理学