Changes

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

**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

**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

**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

**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''

*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

*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