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Synthesis Question: Leishmania Parasites Are Intracellular Protozoa That Causes Skin $\times$

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Synthesis question: Leishmania parasites are intracellular protozoa that causes skin sores, and in some individuals, infections that spread systemically and cause damage to internal organs. In mice, different strains of inbred mice have varying responses to the Leishmania parasite Leishmania major. Whereas C57BL/6 mice develop self-healing skin lesions following infection, Balb/c mice develop non-healing lesions and ultimately succumb to systemic, fatal disease. An example of such data is shown in Figure Q28)A. For these studies, mice were infected with 2 $\times$ 10⁶ L. major promastigotes in the footpad, and the sizes of skin lesions and the numbers of parasites per lesion were measured at the indicated times post-infection. $Synthesis question: Leishmania parasites are intracellular protozoa that causes skin sores, and in some individuals, infections that spread systemically and cause damage to internal organs. In mice, different strains of inbred mice have varying responses to the Leishmania parasite Leishmania major. Whereas C57BL/6 mice develop self-healing skin lesions following infection, Balb/c mice develop non-healing lesions and ultimately succumb to systemic, fatal disease. An example of such data is shown in Figure Q28)A. For these studies, mice were infected with 2 \times 106 L. major promastigotes in the footpad, and the sizes of skin lesions and the numbers of parasites per lesion were measured at the indicated times post-infection. An example of the cytokine data from L. major infected mice is shown in Figure Q28)B. At the indicated times the percentages of CD4 T cells in the draining lymph node producing IFN- \gamma versus IL-4 following stimulation with L. major antigens were measured by intracellular cytokine staining. on TH1 effector T cells, CD8 effector T cells, and NK cells. These chemokines are normally not detectable in healthy tissues, but are strongly up-regulated during infection, injury or inflammation, in response to IFN- \gamma production in the tissue. d) How might this information help explain the divergent ability of C57BL/6 versus Balb/c mice to accumulate increasing numbers of effector T cells into the L. major lesions over the long timecourse shown in the data above?$ An example of the cytokine data from L. major infected mice is shown in Figure Q28)B. At the indicated times the percentages of CD4 T cells in the draining lymph node producing IFN- $\gamma$ versus IL-4 following stimulation with L. major antigens were measured by intracellular cytokine staining. $Synthesis question: Leishmania parasites are intracellular protozoa that causes skin sores, and in some individuals, infections that spread systemically and cause damage to internal organs. In mice, different strains of inbred mice have varying responses to the Leishmania parasite Leishmania major. Whereas C57BL/6 mice develop self-healing skin lesions following infection, Balb/c mice develop non-healing lesions and ultimately succumb to systemic, fatal disease. An example of such data is shown in Figure Q28)A. For these studies, mice were infected with 2 \times 106 L. major promastigotes in the footpad, and the sizes of skin lesions and the numbers of parasites per lesion were measured at the indicated times post-infection. An example of the cytokine data from L. major infected mice is shown in Figure Q28)B. At the indicated times the percentages of CD4 T cells in the draining lymph node producing IFN- \gamma versus IL-4 following stimulation with L. major antigens were measured by intracellular cytokine staining. on TH1 effector T cells, CD8 effector T cells, and NK cells. These chemokines are normally not detectable in healthy tissues, but are strongly up-regulated during infection, injury or inflammation, in response to IFN- \gamma production in the tissue. d) How might this information help explain the divergent ability of C57BL/6 versus Balb/c mice to accumulate increasing numbers of effector T cells into the L. major lesions over the long timecourse shown in the data above?$
on T_H1 effector T cells, CD8 effector T cells, and NK cells. These chemokines are normally not detectable in healthy tissues, but are strongly up-regulated during infection, injury or inflammation, in response to IFN- $\gamma$ production in the tissue.
d) How might this information help explain the divergent ability of C57BL/6 versus Balb/c mice to accumulate increasing numbers of effector T cells into the L. major lesions over the long timecourse shown in the data above?

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Synthesis Question: Leishmania Parasites Are Intracellular Protozoa That Causes Skin ×\times×

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Synthesis Question: Leishmania Parasites Are Intracellular Protozoa That Causes Skin $\times$