495
edits
Changes
→Adaptive Immunity
==Innate Immunity==
==Innate Immunity==
[[File:Helminth Killing edit.png|300px|right|thumb|Helminth Killing - R.J.Francis, RVC 2012]]
[[File:Helmith Killing by Granulocytes.png|250px|right|thumb|Electron Micrograph of Helminth Killing by Granulocytes (G). Adapted from [[http://eprints.adm.unipi.it/527/]] - R.J.Francis, RVC 2012]]
The first line of defence against parasitic infection are the effector mechanisms of the innate immune system. The '''[[Macrophages|macrophages]]''' are important players in the defence against extracellular parasites. This is because macrophages are able to secrete [[Cytokines|cytokines]] as well as perform [[Phagocytosis|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 by mechanisms using free radicals and O<sub>2</sub>-independent toxins (e.g. nitric oxide).
The first line of defence against parasitic infection are the effector mechanisms of the innate immune system. The '''[[Macrophages|macrophages]]''' are important players in the defence against extracellular parasites. This is because macrophages are able to secrete [[Cytokines|cytokines]] as well as perform [[Phagocytosis|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 by mechanisms using free radicals and O<sub>2</sub>-independent toxins (e.g. nitric oxide).
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*Activating [[Complement|complement]], and the subsequent Membrane Attack Complex
*Activating [[Complement|complement]], and the subsequent Membrane Attack Complex
*Blocking attachment to host cells
*Blocking attachment to host cells
*Enhancing macrophage phagocytosis
*Enhancing macrophage [[Phagocytosis|phagocytosis]]
*Involvement in antibody-dependent cell-mediated cytotoxicity
*Involvement in antibody-dependent cell-mediated cytotoxicity
=='''Immunopathology'''==
=='''Immunopathology'''==
The immunopathology is the damage resulting from an immune response to the parasites. Examples include:
*The increase in macrophages and lymphocytes in the liver and spleen can lead to swelling of these organs, e.g. visceral leishmaniasis
*The increase in macrophages and lymphocytes in the liver and spleen can lead to swelling of these organs, e.g. visceral leishmaniasis
*T-cell dependent granulomas forming in organs, e.g. schistosomiasis in the liver
*T-cell dependent (T<sub>H</sub>1 and T<sub>H</sub>17) granulomas forming in organs, e.g. schistosomiasis in the liver
*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