Abstract
Lymphokines (LKY) are non-antibody-soluble products of activated lymphocytes, thought to be mediators of cell mediated immunity. They include putative inflammatory mediators of delayed hypersensitivity such as skin reactive factor. Although they have a number of in vivoand in vitroeffects, the interaction of LKY with macrophages as their target cell has been best studied. The ability of migration inhibitory factor (MIF) reversibly to decrease the spontaneous migration of macrophages in vitrois the basis of the most widely used assay system for lymphokine activity. Despite much work the exact molecular mechanism of MIF action is not known, although recent work is encouraging. It has been known for some time that MIF containing lymphocyte culture supernatants will aggregate macrophages; this was first studied systematically by Lolekha et al 1. These authors showed that macrophage aggregating factor (MAF) was produced by activated lymphocytes under the same conditions as was MIF. Both the aggregation of normal macrophages by preformed LKY (indirect) or the aggregation of sensitized PEC (peritoneal exudate cells, containing both macrophages and lymphocytes) by specific antigen (direct) was observed. The production of MAF and the direct aggregation of sensitized PEC was found to correlate with the state of delayed hypersensitivity in the guinea pig.
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Badenoch-Jones, P., Rouveix, B., Turk, J.L. (1980). The possible role of divalent cations, microtubules and cyclic nucleotides in lymphokine induced macrophage aggregation. In: Willoughby, D.A., Giroud, J.P. (eds) Inflammation: Mechanisms and Treatment. Inflammation: Mechanisms and Treatment, vol 4. Springer, Dordrecht. https://doi.org/10.1007/978-94-010-9423-8_37
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DOI: https://doi.org/10.1007/978-94-010-9423-8_37
Publisher Name: Springer, Dordrecht
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