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Text replace - 'IgE' to 'IgE'
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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:
 
*'''Macrophages'''- important in the defence against extracellular parasites, macrophages are able to secrete cytokines as well as perform phagocytosis
 
*'''Macrophages'''- important in the defence against extracellular parasites, macrophages are able to secrete cytokines as well as perform phagocytosis
**Can act as 'killer cells' through antibody-dependent cell-mediated cytotoxicity, e.g. specific IgG/IgE enhances the ability of macrophages to kill schistosomules
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**Can act as 'killer cells' through antibody-dependent cell-mediated cytotoxicity, e.g. specific IgG/[[IgE]] enhances the ability of macrophages to kill schistosomules
 
**The secretion of TNF-alpha:
 
**The secretion of TNF-alpha:
 
***Activates other macrophages
 
***Activates other macrophages
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**Express Fc and complement receptors- can participate in antibody-dependent cell-mediated cytotoxicity
 
**Express Fc and complement receptors- can participate in antibody-dependent cell-mediated cytotoxicity
 
*'''Eosinophils'''- less phagocytic than [[[[Neutrophils|Neutrophils]] - WikiBlood|neutrophils]], but important in the destruction of larger parasites
 
*'''Eosinophils'''- less phagocytic than [[[[Neutrophils|Neutrophils]] - WikiBlood|neutrophils]], but important in the destruction of larger parasites
**Most activity is controlled by antigen-specific mechanisms, e.g. binding to worms coated with IgG/IgE increases degranulation
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**Most activity is controlled by antigen-specific mechanisms, e.g. binding to worms coated with IgG/[[IgE]] increases degranulation
**The killing of some larvae is enhanced by the activity of mast cells, e.g. antigens released by S. mansoni cause IgE-dependent degranulation of mast cells, the products of which selectively attract eosinophils
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**The killing of some larvae is enhanced by the activity of mast cells, e.g. antigens released by S. mansoni cause [[IgE]]-dependent degranulation of mast cells, the products of which selectively attract eosinophils
 
*'''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''
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*The pathology of elephantiasis is thought to be due to changes in the adult filariae in the lymphatic system
 
*The pathology of elephantiasis is thought to be due to changes in the adult filariae in the lymphatic system
 
*Formation of immune complexes, e.g. deposition in the kidney during malarial infection
 
*Formation of immune complexes, e.g. deposition in the kidney during malarial infection
*Anaphylactic shock caused by IgE production, e.g. after the rupture of hydatid cysts
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*Anaphylactic shock caused by [[IgE]] production, e.g. after the rupture of hydatid cysts
 
*Cross-reaction of antibodies with host tissue, e.g. ''O. volvulus'', the cause of river blindness, expresses an antigen similar to a protein in the retina
 
*Cross-reaction of antibodies with host tissue, e.g. ''O. volvulus'', the cause of river blindness, expresses an antigen similar to a protein in the retina
 
*Excessive production of cytokines, such as TNF-alpha, may contribute to pathology of diseases such as malaria
 
*Excessive production of cytokines, such as TNF-alpha, may contribute to pathology of diseases such as malaria