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→Innate Immunity
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.
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.
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).
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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.
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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 receptors so can participate in antibody-dependent cell-mediated cytotoxicity and [[Phagocytosis|phagocytosis]].
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*'''Platelets'''- cytotoxic activity is increased by cytokines such as TNF-alpha and IFN-γ
*'''Platelets'''- cytotoxic activity is increased by cytokines such as TNF-alpha and IFN-γ
**Potential targets include the larval stage of flukes, e.g. ''T. gondii'' and ''T. cruzi''
**Potential targets include the larval stage of flukes, e.g. ''T. gondii'' and ''T. cruzi''