Abstract
Protozoan parasites of the genus Leishmania escape from the immune response by interfering with signal transduction pathways of its host cell, the macrophage, thereby establishing permissive conditions for intracellular survival. Inhibition of macrophage activation after Leishmania infection has been suggested to require activation of the host cell phosphatase SHP-1. However, by utilizing infections of SHP-1 deficient (me(v)) and CD45 null mutant mice or macrophages, we provide evidence that intracellular survival of Leishmania major is not generally dependent on these cellular phosphatases.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Cells, Cultured
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Female
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Leishmania major / immunology
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Leishmania major / pathogenicity
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Leishmania major / physiology*
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Leishmaniasis, Cutaneous / enzymology
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Leishmaniasis, Cutaneous / immunology
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Leishmaniasis, Cutaneous / parasitology*
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Leukocyte Common Antigens / deficiency*
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Macrophage Activation / physiology
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Macrophages, Peritoneal / immunology
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Macrophages, Peritoneal / parasitology*
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Mice
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Mice, Inbred C57BL
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Mice, Mutant Strains
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Nitric Oxide / metabolism
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Protein Tyrosine Phosphatase, Non-Receptor Type 6 / deficiency*
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Signal Transduction / physiology
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Virulence
Substances
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Nitric Oxide
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Leukocyte Common Antigens
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Protein Tyrosine Phosphatase, Non-Receptor Type 6