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From the Department of Immunology, Royal Postgraduate Medical School, London W.12, and the Department of Medicine, The Division of the Biological Sciences and the Pritzker School of Medicine, University of Chicago, Chicago, Illinois
Abstract
A partially purified "lymphokine" preparation derived from concanavalin A-stimulated human lymphoid cells inhibited macrophage migration in vitro. Intradermal injection of this material into 55 human volunteers produced erythema and induration typical of delayed hypersensitivity except that the response was accelerated. It began after 4 to 6 hr, was maximally indurated after 16 to 20 hr, and subsided within 36 hr. Skin window tests revealed that the glass adherent cells of this reaction were predominantly macrophages as early as 5 to 6 hr after application of the preparation under the coverslips. By contrast, 10 to 24 hr were needed for this degree of macrophage accumulation when antigens were used. Thus, when compared with antigens, the mononuclear phase of the lymphokine reaction was accelerated to a similar extent as was the inflammatory response. A control preparation derived from unstimulated lymphocytes had no migration inhibitory activity and it produced a slight inflammatory reaction, notably erythema.
This observation is in keeping with the idea that lymphocytes are capable of producing factors which preferentially attract monocytes to the site of antigenic stimulation. It also suggests that production of lymphokines, responsible for the accumulation of macrophages, may be a rate-limiting step early in the delayed hypersensitivity reaction.
The migration inhibitory factor active material was used for analyzing skin anergy. Two patients with granulomatous candidiasis and skin anergy failed to develop an inflammatory response to the preparation. Similarly, of eight tuberculin negative patients with sarcoidosis, six failed to respond. Most of these patients responded, however, when the material was injected together with cortisone.
Footnotes
1 Presented in a preliminary form at the American Federation for Clinical Research Meeting, Atlantic City, April, 1972.
This work was supported by the Vigdis and Olafur Memorial Fund in Iceland and the Louis Block Fund, University of Chicago.
2 H.V. is a Wellcome Research Fellow.
3 This work was largely performed while N.S.G. was a visitor at the Royal Postgraduate Medical School, London
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