Type IV or delayed type of hypersensitivity is a bit different because unlike type I & type II hypersensitivity which is mediated by antibodies, type IV is mediated by T cells.
The whole response is directed by chemokines and cytokines released by antigen-stimulated Th1 cells.
This is how it goes..
An antigen tries to sneak into your immune system but it is caught by the very efficient antigen presenting cell (APC).
The APC gobbles the antigen up, processes it & presents it on MHC class II molecules.
APCs are transported regional lymph nodes where Th1 cells are activated by the antigen.
The sensitization phase takes 1-2 weeks, and it this period, Th cells are activated and clonally expanded.
(An army of Th cells is being made *evil laugh*)
Everybody is living happy now until the same antigen tries to sneak into your immune system..
It is caught by the very efficient antigen presenting cell (APC), again.
The APC does the usual, gobbles the antigen up, processes it & presents it on MHC class II molecules.
This uptake, processing, and presentation of the antigen by local APCs is the first phase of delayed type of hypersensitivity.
In the second phase, Th1 cells that have been primed by a previous exposure to the same antigen migrate and become activated.
(We slowly summon the clone army that we have prepared *muhahaha*)
But because there is little inflammation to attract cells into the site, it can take several hours for a T cell of the correct specificity to arrive.
The Th1 cell secretes mediators that activate local endothelial cells, recruiting a macrophage dominated inflammatory cell infiltrate and causes the accumulation of fluid and protein.
(The small & smart army of Th1 cells is now summoning the fighter cops (macrophages).. How cool!)
The chemokines and cytokines released by the Th1 cell grab the attention of your average macrophage (hanging around, probably having a donut) and make them run to the site of antigen to catch the evil antigens!
At this point, after about 24-48 hours, the inflammatory lesion becomes apparent.
Hence the name, "Delayed" type of hypersensitivity.
All these cops (macrophages) amplify the whole "search for antigens & kill em" response.
The influx and activation of macrophages is important in host defense against parasites and bacteria that live within cells, where circulating antibodies cannot reach them.
(Antibodies are small bullets, they can't penetrate the antigen's house.)
Activated macrophages have a heightened phagocytic activity & release a lot of lytic enzymes, which can lead to nonspecific destruction of cells, in the area of infection and thus of the intracellular pathogen.
(It's like a bomb blast, destroying the building in which the terrorist resides!)
Generally, the pathogen is cleared rapidly with little tissue damage.
And everybody lives happily ever after until the same antigen appears again..
The whole response is directed by chemokines and cytokines released by antigen-stimulated Th1 cells.
This is how it goes..
An antigen tries to sneak into your immune system but it is caught by the very efficient antigen presenting cell (APC).
The APC gobbles the antigen up, processes it & presents it on MHC class II molecules.
APCs are transported regional lymph nodes where Th1 cells are activated by the antigen.
The sensitization phase takes 1-2 weeks, and it this period, Th cells are activated and clonally expanded.
(An army of Th cells is being made *evil laugh*)
Everybody is living happy now until the same antigen tries to sneak into your immune system..
It is caught by the very efficient antigen presenting cell (APC), again.
The APC does the usual, gobbles the antigen up, processes it & presents it on MHC class II molecules.
This uptake, processing, and presentation of the antigen by local APCs is the first phase of delayed type of hypersensitivity.
 |
| Antigen presentation - First phase of the delayed type of hypersensitivity response |
(We slowly summon the clone army that we have prepared *muhahaha*)
But because there is little inflammation to attract cells into the site, it can take several hours for a T cell of the correct specificity to arrive.
 |
| In the second phase, Th1 cells migrate and become activated. |
The Th1 cell secretes mediators that activate local endothelial cells, recruiting a macrophage dominated inflammatory cell infiltrate and causes the accumulation of fluid and protein.
(The small & smart army of Th1 cells is now summoning the fighter cops (macrophages).. How cool!)
The chemokines and cytokines released by the Th1 cell grab the attention of your average macrophage (hanging around, probably having a donut) and make them run to the site of antigen to catch the evil antigens!
At this point, after about 24-48 hours, the inflammatory lesion becomes apparent.
Hence the name, "Delayed" type of hypersensitivity.
 |
| Th1 cell secretes chemokines & cytokines that recruit phagocytes (Third phase) |
All these cops (macrophages) amplify the whole "search for antigens & kill em" response.
The influx and activation of macrophages is important in host defense against parasites and bacteria that live within cells, where circulating antibodies cannot reach them.
(Antibodies are small bullets, they can't penetrate the antigen's house.)
Activated macrophages have a heightened phagocytic activity & release a lot of lytic enzymes, which can lead to nonspecific destruction of cells, in the area of infection and thus of the intracellular pathogen.
(It's like a bomb blast, destroying the building in which the terrorist resides!)
Generally, the pathogen is cleared rapidly with little tissue damage.
And everybody lives happily ever after until the same antigen appears again..
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