Difference between revisions of "Adaptive Immunity to Parasites"
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| + | ==Overview== | ||
| + | The role of the adaptive immune system in parasitic infections is mainly to orchestrate the innate immune reactions to the parasites by producing a specific immune response. This could be done either through the cell-mediated response or through the humoral, antibody response. An important note is that the information given here is generalised as the response to each individual parasite is different as parasites themselves range from parasitc worms to malaria (for more information see the Parasitology section of WikiVet). | ||
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==Cell-Mediated== | ==Cell-Mediated== | ||
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> 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 [[Major Histocompatability Complexes|MHC]] class I), while CD8<sup>+</sup> cells are required to mediate immunity against the liver stage (hepatocytes do not express [[Major Histocompatability Complexes|MHC]] class II). | + | *Both CD4<sup>+</sup> T helper cells and CD8<sup>+</sup> cytotoxic T cells are required for protection, e.g CD4<sup>+</sup> cells protect against the blood stage of a Plasmodium infection (erythrocytes do not express [[Major Histocompatability Complexes|MHC]] class I), while CD8<sup>+</sup> cells are required to mediate immunity against the liver stage (hepatocytes do not express [[Major Histocompatability Complexes|MHC]] class II). |
*T<sub>H</sub>1 cells are required to fight intracellular protozoa - the release of Interferon-γ (IFNγ) activates macrophages to kill the protozoa residing within them | *T<sub>H</sub>1 cells are required to fight intracellular protozoa - the release of Interferon-γ (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 Interleuken-5 (IL-5), predominate. IL-5 is the [[Cytokines|cytokine]] responsible for the eosinophilia associated with parasite infections. | *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 Interleuken-5 (IL-5), predominate. IL-5 is the [[Cytokines|cytokine]] responsible for the eosinophilia associated with parasite infections. | ||
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==Humoral== | ==Humoral== | ||
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While cell-mediated immunity is important in tissue infections, such as Leishmania, specific antibodies are important in controlling parasites that live in the bloodstream, e.g. malaria. Mechanisms of antibody-mediated immunity include: | While cell-mediated immunity is important in tissue infections, such as Leishmania, specific antibodies are important in controlling parasites that live in the bloodstream, e.g. malaria. Mechanisms of antibody-mediated immunity include: | ||
*Directly damaging protozoa | *Directly damaging protozoa | ||
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*Enhancing macrophage phagocytosis | *Enhancing macrophage phagocytosis | ||
*Involvement in antibody-dependent cell-mediated cytotoxicity | *Involvement in antibody-dependent cell-mediated cytotoxicity | ||
| − | The humoral response to parasitic worms involves the production of [[Immunoglobulin E|IgE]]. It is stimulated by [[Mast Cells|mast cells]] producing IL-4 ([[Innate Immune System|innate response]]) | + | The humoral response to parasitic worms involves the production of [[Immunoglobulin E|IgE]]. It is stimulated by [[Mast Cells|mast cells]] producing IL-4 ([[Innate Immune System|innate response]]) which causes isotype switching of [[Lymphocytes#B Cells|B cells]] to produce [[Immunoglobulin E|IgE]]. |
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{{Jim Bee 2007}} | {{Jim Bee 2007}} | ||
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[[Category:Adaptive Immune System]] | [[Category:Adaptive Immune System]] | ||
Latest revision as of 16:14, 2 July 2012
Overview
The role of the adaptive immune system in parasitic infections is mainly to orchestrate the innate immune reactions to the parasites by producing a specific immune response. This could be done either through the cell-mediated response or through the humoral, antibody response. An important note is that the information given here is generalised as the response to each individual parasite is different as parasites themselves range from parasitc worms to malaria (for more information see the Parasitology section of WikiVet).
Cell-Mediated
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+ T helper cells and CD8+ cytotoxic T 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 Interferon-γ (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 Interleuken-5 (IL-5), predominate. IL-5 is the cytokine 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
While cell-mediated immunity is important in tissue infections, such as Leishmania, specific antibodies are important in controlling parasites that live in the bloodstream, e.g. malaria. Mechanisms of antibody-mediated immunity include:
- Directly damaging protozoa
- Activating complement, and the subsequent Membrane Attack Complex
- Blocking attachment to host cells
- Enhancing macrophage phagocytosis
- Involvement in antibody-dependent cell-mediated cytotoxicity
The humoral response to parasitic worms involves the production of IgE. It is stimulated by mast cells producing IL-4 (innate response) which causes 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 |
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