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The first line of defence against parasitic infection are the effector mechanisms of the innate immune system.
 
The first line of defence against parasitic infection are the effector mechanisms of the innate immune system.
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The '''[[Macrophages|Macrophages]]''' are important in the defence against extracellular parasites. This is because macrophages are able to secrete [[Cytokines|cytokines]] as well as perform phagocytosis. In this they can act as 'killer cells' through antibody-dependent cell-mediated cytotoxicity, for example specific [[Immunoglobulins|IgG]]/[[Immunoglobulins|IgE]] enhances the ability of macrophages to kill schistosomules through the interaction of Fc receptors on the surface of the macrophage. Of the secreted cytokines, the secretion of TNF-&alpha& is of particular importance. This is because TNF-&alpha& activates other macrophages and can have toxic effects in high amounts. TNF-alpha also renders hepatocytes resistant to malarial infection when in conjunction with IL-1.
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The '''[[Macrophages|Macrophages]]''' are important in the defence against extracellular parasites. This is because macrophages are able to secrete [[Cytokines|cytokines]] as well as perform phagocytosis. In this they can act as 'killer cells' through antibody-dependent cell-mediated cytotoxicity, for example specific [[Immunoglobulins|IgG]]/[[Immunoglobulins|IgE]] enhances the ability of macrophages to kill schistosomules through the interaction of Fc receptors on the surface of the macrophage. Of the secreted cytokines, the secretion of TNFα is of particular importance. This is because TNFα activates other macrophages and can have toxic effects in high amounts. TNFα also renders hepatocytes resistant to malarial infection when in conjunction with IL-1. Cytokine secretion (in particular IFNγ) can also enhance killing mechanisms using free radicals and O<sub>2</sub>-independent toxins (e.g. nitric oxide) are enhanced.
*****When activated by cytokines, killing mechanisms using free radicals and O2-independent toxins (e.g. nitric oxide) are enhanced
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*'''[[Neutrophils|Neutrophils]]'''- similar properties to macrophages
 
*'''[[Neutrophils|Neutrophils]]'''- similar properties to macrophages
 
**Activated by cytokines such as TNF-alpha, IFN-γ and GM-CSF, [[Neutrophils|Neutrophils]] produce a more intense respiratory burst and extracellular killing is mediated by H2O2
 
**Activated by cytokines such as TNF-alpha, IFN-γ and GM-CSF, [[Neutrophils|Neutrophils]] produce a more intense respiratory burst and extracellular killing is mediated by H2O2
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