Trypanosoma cruzi: T-cell-dependent mechanisms of resistance during chronic infection
| Autor: | Marta A. Lauricella, Angel Sinagra, Rita L. Cardoni, Elsa L. Segura, Irene Rodriguez Nantes, Adelina Riarte, Martin E. Rottenberg |
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| Rok vydání: | 1991 |
| Předmět: |
Interleukin 2
Male Cellular immunity T cell T-Lymphocytes Trypanosoma cruzi Immunology Spleen Cyclosporins Parasitemia Biology Lymphocyte Activation Microbiology Interferon-gamma Mice Cyclosporin a medicine Animals Interferon gamma Chagas Disease Cells Cultured Mice Inbred BALB C Macrophages General Medicine Macrophage Activation biology.organism_classification medicine.disease Infectious Diseases medicine.anatomical_structure Immunoglobulin G Interleukin-2 Parasitology medicine.drug |
| Zdroj: | Experimental parasitology. 73(2) |
| ISSN: | 0014-4894 |
| Popis: | Effector mechanisms of resistance exerted by T cells from BALB/c mice chronically infected with Trypanosoma cruzi, Tulahuen strain, were studied. Spleen cells from chronically infected mice (Chro-SC) prestimulated with heat-killed trypomastigotes (HKT) and/or IL-2 destroyed PHA-labeled p-815 mastocytoma cells, HKT-pulsed macrophages, and normal peritoneal macrophages. However, HKT-stimulated Chro-SC did not affect the infectivity of free bloodstream forms of the parasite. Upon HKT stimulation, Chro-SC or their culture supernatant activated peritoneal macrophages for the destruction of intracellular amastigotes. The effect was abolished after Thy 1.2+ cell depletion. The addition of Cyclosporin A (CyA), which blocks T-cell activation, during HKT-stimulation of Chro-SC, diminished their ability to activate the trypanocidal activity of macrophages. CyA also inhibited the production of both macrophage-activating factors and interferon-gamma by HKT-stimulated Chro-SC. CyA administration to recipients of nylon-wool nonadherent spleen cells from chronically infected mice inhibited their adoptively acquired resistance against T. cruzi, suggesting that the conferred resistance depended on the effect of specifically activated cells. When administered during the chronic stage of the infection, CyA abrogated the antigen-specific delayed type hypersensitivity response but increased the levels of anti-T. cruzi IgG antibodies. Neither parasitemia, tissular parasitism in myocardium or skeletal muscle, nor mortality were detected after CyA treatment, suggesting the presence of a CyA nonsensitive mechanism(s) in the control of T. cruzi during the chronic phase of the infection. |
| Databáze: | OpenAIRE |
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