THE OUTCOME OF THE PARASITIC PROCESS INITIATED BY LEISHMANIA-INFANTUMIN LABORATORY MICE - A TISSUE-DEPENDENT PATTERN CONTROLLED BY THE LSHAND MHC LOCI

Human visceral leishmaniasis is mainly due to intracellular protozoan parasites of the Leishmania donovani complex, i.e., L. donovani and L. infantum (or L. chagasi). A mouse model has been established to monit or 1) the parasitic process initiated by L. infantum in three tissues they invade, and 2) parameters of the acquired immune response they tr igger. Mice congenic at the Lsh locus and mice of inbred strains diffe ring at the MHC locus have been inoculated by the i.v. route with L. i nfantum, The parasitic process has been evaluated by the follow-up of the parasitic load in the liver, the spleen, and, for the first time, in the bone marrow using a very sensitive limiting dilution assay, As previously established for L. donovani, the early outcome of L. infant um is also under the control of the Lsh locus in the liver; genes of t he MHC complex are involved in the development of the subsequent acqui red immune response, ''Cure'' or ''noncure'' haplotypes are the same f or the two species of Leishmania; as far as the cure haplotype is conc erned, whatever the tissues being screened, the parasites are never to tally cleared, although the liver is the tissue in which the best para site load reduction is achieved, Through immunostaining, it was establ ished that sialoadhesin-positive stromal bone marrow macrophages conta in parasites; such long-lived mononuclear phagocytes could be the host cells where the parasite can find ''safe targets'' unreactive to the dominant effector immune mechanism triggered by the replicative stage of the parasites.