Adaptive Immunity to Parasites - Revision history

Bara at 16:14, 2 July 2012

2012-07-02T16:14:22Z

Rjfrancisrvc: /* Humoral */

2012-05-28T11:43:51Z

Humoral

Rjfrancisrvc: /* Cell-Mediated */

2012-05-18T09:28:23Z

Cell-Mediated

Rjfrancisrvc: /* Overview */

2012-05-18T09:26:04Z

Overview

Rjfrancisrvc at 09:25, 18 May 2012

2012-05-18T09:25:19Z

Rjfrancisrvc: /* Humoral */

2012-05-18T09:20:00Z

Humoral

Rjfrancisrvc: /* Cell-Mediated */

2012-05-18T09:18:11Z

Cell-Mediated

Rjfrancisrvc: /* Cell-Mediated */

2012-05-18T09:16:57Z

Cell-Mediated

Rjfrancisrvc at 09:16, 18 May 2012

2012-05-18T09:16:44Z

Rjfrancisrvc: /* Humoral */

2012-05-18T09:11:09Z

Humoral

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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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 {{Jim Bee 2007}}
 [[Category:Adaptive Immune System]]

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 *Enhancing macrophage phagocytosis
 *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]]). It also includes isotype switching of [[Lymphocytes#B Cells|B cells]] to produce [[Immunoglobulin E|IgE]].
+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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 ==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''.
-*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
 *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.

@@ Line 1: / Line 1: @@
 ==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 immune 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).
+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|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''.

@@ Line 1: / Line 1: @@
 ==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''.
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 ==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

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 *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 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 [[Cytokine|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.
 *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]]

← Older revision		Revision as of 09:11, 18 May 2012
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	==Humoral==		==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\|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 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]].		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]].