
doi: 10.2741/a353
pmid: 9820738
The host-pathogen relationship is the focus of many different studies which use a variety of disease models and different pathogens. Immunological studies in the mouse using the intracellular parasite Leishmania have helped define several aspects of host-pathogen interactions. Resistance to Leishmania is dependent on the development of CD4+ Th1 cells which promote an effective cell mediated immune response. Production of the cytokine IFN-gamma during this immune response activates macrophages enabling them to kill the parasite and control the infection. In contrast, susceptibility to this parasite is characterized by a Th2 response which produces predominantly IL-4. This cytokine promotes high antibody titers directed towards the parasite but does not activate macrophages for parasite killing. This host response results in high parasite numbers and a progressive increase in lesion size. The mouse model of leishmaniasis has been extremely useful in gaining an understanding of the immunological factors important in determining T cell commitment into Th1 or Th2 populations during an in vivo immune response.
Leishmania, Immunity, Cellular, Mice, Inbred BALB C, Macrophages, T-Lymphocytes, Leishmaniasis, Cutaneous, Th1 Cells, Interleukin-12, Immunity, Innate, Host-Parasite Interactions, Mice, Th2 Cells, Animals, Cytokines, Humans, Disease Susceptibility
Leishmania, Immunity, Cellular, Mice, Inbred BALB C, Macrophages, T-Lymphocytes, Leishmaniasis, Cutaneous, Th1 Cells, Interleukin-12, Immunity, Innate, Host-Parasite Interactions, Mice, Th2 Cells, Animals, Cytokines, Humans, Disease Susceptibility
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