Difference between revisions of "Adaptive Immunity to Parasites"
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==Overview== | ==Overview== | ||
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Although the innate immune system provides an effective first line of defence, '''[[T cells|T cells]]''' are fundamental in the development of immunity, demonstrated using T-cell deprived mice that fail to resolve otherwise non-lethal infections of, for example, ''T. cruzi''. | Although the innate immune system provides an effective first line of defence, '''[[T cells|T cells]]''' are fundamental in the development of immunity, demonstrated using T-cell deprived mice that fail to resolve otherwise non-lethal infections of, for example, ''T. cruzi''. | ||
| − | *Both CD4<sup>+</sup> | + | *Both CD4<sup>+</sup> and CD8<sup>+</sup> cells are required for protection, e.g CD4<sup>+</sup> cells protect against the blood stage of a Plasmodium infection (erythrocytes do not express MHC class I), while CD8<sup>+</sup> cells are required to mediate immunity against the liver stage (hepatocytes do not express MHC class II). |
| − | *T<sub>H</sub>1 cells are required to fight intracellular protozoa - the release of | + | *T<sub>H</sub>1 cells are required to fight intracellular protozoa - the release of IFNγ activates macrophages to kill the protozoa residing within them |
| − | *Helminth infections require both T<sub>H</sub>1 and T<sub>H</sub>2 responses, e.g. during ''S. mansoni'' the secretion of IFNγ by T<sub>H</sub>1 cells activates mechanisms that destroy larvae in the lungs, although the T<sub>H</sub>2 subset, secreting | + | *Helminth infections require both T<sub>H</sub>1 and T<sub>H</sub>2 responses, e.g. during ''S. mansoni'' the secretion of IFNγ by T<sub>H</sub>1 cells activates mechanisms that destroy larvae in the lungs, although the T<sub>H</sub>2 subset, secreting IL-5, predominate. IL-5 is responsible for the eosinophilia associated with parasite infections. |
*T<sub>H</sub>2 cells are required for the destruction of intestinal worms, where they induce mucosal mast cells and interact with [[Eosinophils|eosinophils]] | *T<sub>H</sub>2 cells are required for the destruction of intestinal worms, where they induce mucosal mast cells and interact with [[Eosinophils|eosinophils]] | ||
==Humoral== | ==Humoral== | ||
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| − | + | The humoral response involves the production of [[Immunoglobulin E|IgE]]. It is stimulated by [[Mast Cells|mast cells]] producing IL-4 ([[Innate Immune System|innate response]]). It also includes isotype switching of [[Lymphocytes#B Cells|B cells]] to produce [[Immunoglobulin E|IgE]]. | |
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| − | The humoral response | ||
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{{Jim Bee 2007}} | {{Jim Bee 2007}} | ||
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[[Category:Adaptive Immune System]] | [[Category:Adaptive Immune System]] | ||
Revision as of 09:10, 18 May 2012
Overview
Although the innate immune system provides an effective first line of defence, T cells are fundamental in the development of immunity, demonstrated using T-cell deprived mice that fail to resolve otherwise non-lethal infections of, for example, T. cruzi.
- Both CD4+ and CD8+ cells are required for protection, e.g CD4+ cells protect against the blood stage of a Plasmodium infection (erythrocytes do not express MHC class I), while CD8+ cells are required to mediate immunity against the liver stage (hepatocytes do not express MHC class II).
- TH1 cells are required to fight intracellular protozoa - the release of IFNγ activates macrophages to kill the protozoa residing within them
- Helminth infections require both TH1 and TH2 responses, e.g. during S. mansoni the secretion of IFNγ by TH1 cells activates mechanisms that destroy larvae in the lungs, although the TH2 subset, secreting IL-5, predominate. IL-5 is responsible for the eosinophilia associated with parasite infections.
- TH2 cells are required for the destruction of intestinal worms, where they induce mucosal mast cells and interact with eosinophils
Humoral
The humoral response involves the production of IgE. It is stimulated by mast cells producing IL-4 (innate response). It also includes isotype switching of B cells to produce IgE.
Also see Immunity to Parasites
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Originally funded by the RVC Jim Bee Award 2007 |