Lesional modulation of peripheral monocyte leucotactic responsiveness in leprosy.

Because the accumulation and activation of mononuclear phagocytes are critical to the host response to intracellular microbial pathogens, we evaluated mechanisms of peripheral monocyte leucotactic regulation in leprosy. Plasma from 53 of 67 patients was found to inhibit the locomotion of normal human monocytes. Neither the prevalence nor the magnitude of plasma leucotactic inhibitory activity correlated with disease histology or duration, type or duration of chemotherapy, or history of erythema nodosum leprosum. Plasma leucotactic inhibitory activity resided principally in a non-immunoglobulin, cell-directed inhibitor of 230,000 daltons molecular weight. Fractionation of plasma from patients with lepromatous leprosy revealed an additional, immunoglobulin-containing inhibitor of approximately 400,000 daltons weight, possibly an IgG-IgA immune complex. Production of leucotactic inhibitors by unstimulated and concanavalin A-stimulated peripheral mononuclear cells was normal; however, cutaneous explants from these patients spontaneously produced the 230,000 dalton leucotactic inhibitor in vitro. The ability of the lesions of leprosy to impede monocyte traffic may be an important pathogenetic mechanism.