The TNF Receptors p55 and p75 Mediate Chemotaxis of PMN Induced by TNFα and a TNFα 36–62 Peptide
The 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 p...
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| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
1994-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/S0962935194000487 |
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| Summary: | The 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. |
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| ISSN: | 0962-9351 1466-1861 |