Author(s): Pham TV, MacDonald HR, Maul J
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Abstract Peritoneal macrophages from CBA/T6 (healer) and BALB/c (non-healer) mice were infected with Leishmania major (LV39) in vitro. The microorganism replicated at the same rate in macrophages from either strain. Exposure of infected cells to lymph node cells (LNC) from infected syngeneic animals led to intracellular killing of the parasite by macrophages from both strains, provided LPS was present in the incubation medium. In vitro-propagated L.major-specific T-cell blasts activated macrophages from either strain in the absence of LPS. On a per cell basis, lymphoid cells from BALB/c mice were less efficient, however, than cells from CBA/T6 mice. Lysis of parasitized macrophages was also more marked in CBA/T6 than in BALB/c cell mixtures. LNC exposed to parasite antigen or to infected macrophages secreted macrophage-activating factor (MAF); incubation with antigen also induced lymphocyte proliferation. MAF production and LNC proliferation decreased with progression of the infection of BALB/c mice, but always remained significant. The reduction in relative T-cell numbers in the lymph nodes of infected animals was moderate; the absolute number of T-cells increased markedly in the lymphoid organs of both strains, however. These results suggest that failure to heal may coexist together with active cell-mediated immune response in non-healer mice.
This article was published in Parasite Immunol
and referenced in Journal of Cytokine Biology