THE ROLE OF MACROPHAGE RECEPTORS IN ADHESION AND UPTAKE OF LEISHMANIA-MEXICANA AMASTIGOTES

Amastigotes of the protozoan parasite Leishmania proliferate in phagol ysosomes of mammalian macrophages, Propagation of the infection is con sidered to occur by host-cell rupture and uptake of released parasites by uninfected macrophages, In this study, the kinetics of binding of L, mexicana mexicana amastigotes to COS cells and to COS cells transfe cted with three different macrophage receptors (FcRII-B2, receptor for the Fc-domain of immunoglobulins; CR3, complement type 3 receptor and the mannose receptor) is compared to the rate of adhesion to peritone al macrophages, Amastigotes isolated from macrophages cultivated in vi tro bind with slow, sigmoid kinetics to COS cells expressing either of the three receptors, or to peritoneal macrophages, In contrast, amast igotes isolated from mouse lesions bind with rapid, hyperbolic kinetic s to COS cells expressing the Fc receptor or to peritoneal macrophages but with slow, sigmoid kinetics to COS cells expressing the CR3 or th e mannose receptor, As shown by immunofluorescence experiments, lesion -derived amastigotes contain host-derived immunoglobulins (Ig) but no complement component 3 at their surface, It is concluded that amastigo tes contain no intrinsic ligand at their surface, which enables high-a ffinity interactions with macrophages, Opsonization by specific Ig may be of relevance in vivo because firstly, in cryosections of mouse les ions extracellular amastigotes containing surface Ig can be detected a nd, secondly, B cell-deficient mice reconstituted with parasite-specif ic Ig show a modest increase in the rate of lesion development, In add ition, it is shown that amastigotes are internalized by COS cells and grow in large parasitophorous vacuoles similar to those observed in ma crophages.