Difference between revisions of "Adaptive Immunity to Bacteria"
Rjfrancisrvc (talk | contribs) |
|||
| (One intermediate revision by one other user not shown) | |||
| Line 1: | Line 1: | ||
| − | |||
==Overview== | ==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. | 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. | ||
| Line 15: | Line 14: | ||
==Extracellular Infection== | ==Extracellular Infection== | ||
| − | 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]]. | + | 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]]. | ||
==Vesicular Infection== | ==Vesicular Infection== | ||
| Line 27: | Line 27: | ||
{{Jim Bee 2007}} | {{Jim Bee 2007}} | ||
| − | |||
| − | |||
[[Category:Adaptive Immune System]] | [[Category:Adaptive Immune System]] | ||
Revision as of 11:19, 17 May 2012
Overview
The adaptive and innate responses work together to destroy bacteria. The adaptive response ensures the innate response is carried out efficiently. There are two major branches of the adaptive immune response, humoral immunity and cell-mediated immunity.
Humoral
Humoral immunity includes complement activation of the classical pathway. It results in the production of IgM and IgG and makes the complement system more efficient.
Cell-Mediated
Cell-mediated immunity provides help for macrophages. It includes IgG production (through T-helper type II (TH2) cell interaction with B cells), which improves phagocytosis by opsonisation. Infected macrophages are rescued by T-helper type I (TH1) cells when phagocytosis and digestion mechanisms fail to eliminate the pathogen.
Extracellular Infection
The response to extracellular infection involves complement and phagocytosis; B cell and TH2 cell stimulation and the production of IgM, which activates the classical cascade. TH17 stimulation also enhances extravasation of neutrophils
to the area to clear the pathogen. There is also class switching of IgM to IgG, which is a good opsonin and targets bacterial Fcγ receptor expressed by macrophages and neutrophils.
Vesicular Infection
During a vesicular infection, the infected macrophage secretes IL-12. IL-12 stimulates T-helper type I cells which release IFN-γ. IFN-γ then triggers the macrophages to kill the pathogens inside.
Also see Immunity to Bacteria
|
Originally funded by the RVC Jim Bee Award 2007 |