Difference between revisions of "Adaptive Immunity to Bacteria"

From WikiVet English
Jump to navigation Jump to search
Line 14: 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 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==

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.

Adaptive Immunity to Extracellular Bacteria - R.J.Francis, RVC 2012

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

Adaptive Immunity to Vesicular Bacteria - R.J.Francis, RVC 2012



LIVE logo Originally funded by the RVC Jim Bee Award 2007