immune system
• mice do not mount an effective Th1 response to L. major footpad infection as measured by decreased production of IFN-gamma by CD4 T cells
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• calcium influx of stimulated CD4 T cells is markedly reduced
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• CD 4 T cells stimulated with anti-CD3 antibody proliferate poorly with only 23% of cells undergoing cell division compared to 40% of wild-type controls
• exogenous administration of IL-2 rescues the proliferation defect
• addition of ionomycin also rescues the proliferation defect
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• popliteal CD4 T cells from L. major infected mice secrete up to 10-fold less IFN-gamma than wild-type controls
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• CD 4 T cells stimulated with anti-CD3 antibody for one or two days produce little IL-2
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• popliteal CD4 T cells from L. major infected mice secrete more IL-4 than wild-type controls
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• mice exhibit enhanced lesion development and a 100-fold increase in parasite burden after infection with L. major in the footpad
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hematopoietic system
• mice do not mount an effective Th1 response to L. major footpad infection as measured by decreased production of IFN-gamma by CD4 T cells
|
• calcium influx of stimulated CD4 T cells is markedly reduced
|
• CD 4 T cells stimulated with anti-CD3 antibody proliferate poorly with only 23% of cells undergoing cell division compared to 40% of wild-type controls
• exogenous administration of IL-2 rescues the proliferation defect
• addition of ionomycin also rescues the proliferation defect
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cellular
• CD 4 T cells stimulated with anti-CD3 antibody proliferate poorly with only 23% of cells undergoing cell division compared to 40% of wild-type controls
• exogenous administration of IL-2 rescues the proliferation defect
• addition of ionomycin also rescues the proliferation defect
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