immune system
• the percentage of granulocytes in L. major infected areas is increased 4 fold
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• in L. major infected areas
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• decrease in the percentage of regulatory T cells in the draining lymph nodes after infection with Leishmania major
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• decrease in the percentage of TNF positive CD4+ T cells in L. major infected mice
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• pretreatment of macrophages with IFNG fails to reduce the number of L. major amastigotes within the macrophage unlike in wild-type cells
• uninfected cells produce more nitrite both basally and in response to IFNG stimulation compared to wild-type cells; however, infected cells stimulated with IFNG produce less nitrite compared to infected wild-type cells
• decrease in IFNG stimulated TNF production and L. major infection fails to induce TNF production in macrophages
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• decrease in the number of intracellular amastigotes without concurrence of detectable alteration in the number of adherent, nonopsonized L. major parasites
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• increase in the amount of IL10 and IL17 in L. major infected ears compared to infected wild-type controls
• however, levels of IL12, IL6, and IL4 are similar to infected wild-type controls
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• decrease in the level of TNF in L. major infected ears at 5 days and, to a lesser extent, 7 weeks post infection
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• decrease in IFNG stimulated TNF production and L. major infection fails to induce TNF production in macrophages
• decrease in the percentage of TNF positive CD4+ T cells in L. major infected mice
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• decrease in the percentage of regulatory T cells in the draining lymph nodes after infection with L. major
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• increase in the severity of L. major induced lesions, with infection producing more severe ulcers and a larger inflammatory rim around the epidermal defect
• perforation of L. major infected ears is seen 4 weeks post infection
• healing post infection is delayed by 3 - 4 weeks compared to wild-type controls
• 100-fold increase in L. major parasite load compared to wild-type controls
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cardiovascular system
• significant decrease in cAMP induced vasorelaxation at 1 month of age
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homeostasis/metabolism
• increase in the amount of IL10 and IL17 in L. major infected ears compared to infected wild-type controls
• however, levels of IL12, IL6, and IL4 are similar to infected wild-type controls
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• decrease in the level of TNF in L. major infected ears at 5 days and, to a lesser extent, 7 weeks post infection
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• about a 3 - 4 week delay in healing of L. major infection induced lesions
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hematopoietic system
• the percentage of granulocytes in L. major infected areas is increased 4 fold
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• in L. major infected areas
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• decrease in the percentage of regulatory T cells in the draining lymph nodes after infection with Leishmania major
|
• decrease in the percentage of TNF positive CD4+ T cells in L. major infected mice
|
• pretreatment of macrophages with IFNG fails to reduce the number of L. major amastigotes within the macrophage unlike in wild-type cells
• uninfected cells produce more nitrite both basally and in response to IFNG stimulation compared to wild-type cells; however, infected cells stimulated with IFNG produce less nitrite compared to infected wild-type cells
• decrease in IFNG stimulated TNF production and L. major infection fails to induce TNF production in macrophages
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• decrease in the number of intracellular amastigotes without concurrence of detectable alteration in the number of adherent, nonopsonized L. major parasites
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muscle
• significant decrease in cAMP induced vasorelaxation at 1 month of age
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cellular
• decrease in the number of intracellular amastigotes without concurrence of detectable alteration in the number of adherent, nonopsonized L. major parasites
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