495
edits
Changes
→Innate Immunity
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As well as the macrophages, the granulocytes form the main effector response to parasitic infection. '''[[Eosinophils|Eosinophils]]''' are very important in the destruction of larger parasites even though they are less phagocytic than [[Neutrophils|neutrophils]]. Most activity from eosinophils is controlled by antigen-specific mechanisms, for example binding to worms coated with [[IgG]]/[[IgE]] increases '''degranulation'''. Degranulation, through the process known as '''exocytosis''', releases enzymes that degrade the parasite into smaller chunks so it can be cleared by phagocytosis. The eosinophils also form the end point of the adaptive immune response to larger parasites with the killing of some larvae being enhanced by the activity of mast cells, for example antigens released by ''S. mansoni'' cause IgE-dependent degranulation of mast cells, the products of which selectively attract eosinophils.
As well as the macrophages, the granulocytes form the main effector response to parasitic infection. '''[[Eosinophils|Eosinophils]]''' are very important in the destruction of larger parasites even though they are less phagocytic than [[Neutrophils|neutrophils]]. Most activity from eosinophils is controlled by antigen-specific mechanisms, for example binding to worms coated with [[IgG]]/[[IgE]] increases '''degranulation'''. Degranulation, through the process known as '''exocytosis''', releases enzymes that degrade the parasite into smaller chunks so it can be cleared by phagocytosis. The eosinophils also form the end point of the adaptive immune response to larger parasites with the killing of some larvae being enhanced by the activity of mast cells, for example antigens released by ''S. mansoni'' cause IgE-dependent degranulation of mast cells, the products of which selectively attract eosinophils. Mast cells and eosinophils degranulation enhances the T<sub>H</sub>2 response through the release of [[Cytokines|cytokines]], for example IL-4 and IL-13, that is needed to clear a stubborn infection.
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The other granulocytes present in parasite-infected inflammatory lesions and involved in the anti-parasitic response are the '''[[Neutrophils|neutrophils]]'''. In the parasitic response they have similar properties to macrophages with activation caused by cytokines such as TNFα, IFNγ and GM-CSF. Their mechanism for killing is by an intense respiratory burst, with extracellular killing being mediated by hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>). In addition, they also express Fc and [[Complement|complement]] receptors so can participate in antibody-dependent cell-mediated cytotoxicity and [[Phagocytosis|phagocytosis]].
The other granulocytes present in parasite-infected inflammatory lesions and involved in the anti-parasitic response are the '''[[Neutrophils|neutrophils]]'''. In the parasitic response they have similar properties to macrophages with activation caused by cytokines such as TNFα, IFNγ and GM-CSF. Their mechanism for killing is by an intense respiratory burst, with extracellular killing being mediated by hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>). In addition, they also express Fc and [[Complement|complement]] receptors so can participate in antibody-dependent cell-mediated cytotoxicity and [[Phagocytosis|phagocytosis]]. Due to innate inflammatory mechanisms neutrophils are early responders to parasite infection.
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