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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.

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