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− | *The adaptive and [[Innate Immune System|innate responses]] work together to destroy bacteria
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| + | ==Overview== |
| + | The adaptive and [[Innate Immune System|innate responses]] work together to destroy bacteria. The adaptive response ensures the [[Innate Immune System|innate response]] is carried out efficiently. There are two major branches of the adaptive immune response, humoral immunity and cell-mediated immunity. |
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− | *The adaptive response ensures the [[Innate Immune System|innate response]] is carried out efficiently
| + | [[File:Adaptive Immunity to Extracellular Bacteria.png|thumb|right|300px|Adaptive Immunity to Extracellular Bacteria - R.J.Francis, RVC 2012]] |
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− | '''Humoral'''
| + | ==Humoral== |
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− | *[[Complement|Complement]] activation of the classical pathway
| + | Humoral immunity includes [[Complement|complement]] activation of the classical pathway. It results in the production of [[Immunoglobulin M|IgM]] and [[Immunoglobulin G|IgG]] and makes the complement system more efficient. |
− | **Production of [[Immunoglobulin M|IgM]] and [[Immunoglobulin G|IgG]] makes the complement system more efficient
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− | '''Cell-Mediated'''
| + | ==Cell-Mediated== |
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− | *Help for macrophages
| + | Cell-mediated immunity provides help for macrophages. It includes [[Immunoglobulin G|IgG]] production (through T-helper type II (T<sub>H</sub>2) cell interaction with [[Lymphocytes#B Cells|B cells]]), which improves phagocytosis by opsonisation. Infected [[Macrophages|macrophages]] are rescued by T-helper type I (T<sub>H</sub>1) cells when phagocytosis and digestion mechanisms fail to eliminate the pathogen. |
− | **[[Immunoglobulin G|IgG]] production (T-helper type II cells and [[Lymphocytes#B Cells|B cells]]) which improves phagocytosis by opsonisation
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− | **Infected [[Macrophages|macrophages]] are rescued by T-helper type I cells when phagocytosis and digestion mechanisms fail to eliminate the pathogen
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− | '''Extracellular Infection'''
| + | ==Extracellular Infection== |
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− | *Complement and phagocytosis
| + | The response to extracellular infection involves [[Complement|complement]] and phagocytosis; [[Lymphocytes#B Cells|B cell]] and T<sub>H</sub>2 cell stimulation and the production of [[Immunoglobulin M|IgM]], which activates the classical cascade. T<sub>H</sub>17 stimulation also enhances extravasation of [[Neutrophils|neutrophils]] to the area to clear the pathogen. There is also class switching of [[Immunoglobulin M|IgM]] to [[Immunoglobulin G|IgG]], which is a good opsonin and targets bacterial Fcγ receptor expressed by [[Macrophages|macrophages]] and [[Neutrophils|neutrophils]]. |
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− | *[[Lymphocytes#B Cells|B cell]] and T helper type II cell stimulation
| + | ==Vesicular Infection== |
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− | *Production of [[Immunoglobulin M|IgM]] which activates the classical cascade
| + | During a vesicular infection, the infected [[Macrophages|macrophage]] secretes IL-12. IL-12 stimulates T-helper type I cells which release IFN-γ. IFN-γ then triggers the [[Macrophages|macrophages]] to kill the pathogens inside. |
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− | *Class switching of [[Immunoglobulin M|IgM]] to [[Immunoglobulin G|IgG]] which is a good opsonin and targets bacterial Fcγ receptor expressed by [[Macrophages|macrophages]] and [[Neutrophils|neutrophils]]
| + | <big>'''Also see [[Immunity to Bacteria]]'''</big> |
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− | '''Vesicular Infection'''
| + | [[File:Adaptive Immunity to Intracellular Bacteria.png|thumb|right|300px|Adaptive Immunity to Vesicular Bacteria - R.J.Francis, RVC 2012]] |
| + | <br><br> |
| + | {{Jim Bee 2007}} |
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− | *The infected [[Macrophages|macrophage]] secretes IL-12
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− | *IL-12 stimulates T-helper type I cells which release IFN-γ
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− | | + | [[Category:Adaptive Immune System]] |
− | *IFN-γ triggers the [[Macrophages|macrophages]] to kill the pathogens inside
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− | [[Category:To Do - Blood]] | |