Allergic Cascade (cont.)
In this Article
What about a more detailed look at the "players?"
- T's & B's
Once the IgE is produced, it specifically recognizes the ragweed pollen and will recognize it on future exposure.
The balance between allergy-promoting TH2 cells and infection-fighting TH1 cells has recently been found to be a critical component of our immune system. Whereas allergy reactions involve large numbers of TH2 cells, infections generate an army of TH1 cells, which then release chemicals that help destroy microbes.
Allergy and asthma rates have been increasing in recent decades. One currently favored theory explaining the increase is that it is a consequence of inadequately "geared up" human immune systems because of the relatively sterilized environment of modern man, possibly due to antibiotics and vaccinations! This has been referred to as the "hygiene hypothesis." What this concept implies is that the immune systems of individuals who have been exposed to sufficient microbes make TH1 cells when stimulated. But, if an individual's immune system is inadequately stimulated to produce TH1 cells by exposure to microbes, it will instead lean toward the allergy-producing system and make TH2 cells. A tendency toward allergic reactions is the result.
Although this appears complicated, an understanding of the different lymphocyte responses is important in treating allergies. Ideally, we would like to respond to ragweed pollen with TH1 lymphocytes and not TH2 lymphocytes, which promote allergic reactions and produce IgE in large amounts. Allergic individuals summon a large number of TH2 cells in response to allergens, whereas non-allergic people do not.
Finally, the tendency to develop allergic conditions (i.e., to develop strong TH2 responses to allergens) is thought to be partially inherited from our parents. At birth, there seems to be a balance between the infection-fighting TH1 cells and the allergy-promoting TH2 cells. Current thinking is that allergy develops after birth when a child is exposed to certain substances in the environment. The immune system is stimulated by these exposures so that the scales are now tipped toward the production of allergy-promoting TH2 cells. They are especially tipped toward allergy promotion in individuals that have inherited the genetic tendency from their parents.
Mast Cells & Basophils
Some chemical mediators are not formed until 5 to 30 minutes after activation of the mast cells or basophils. The most prominent of these are the leukotrienes. Leukotriene D4 is 10 times more potent than histamine. Its effects are similar to those of histamine, but leukotriene D4 also attracts other cells to tarea, thereby aggravating the inflammation.
The other group of inflammation-causing chemical mediators that form after mast cell stimulation is the prostaglandins. Prostaglandin D2, in particular, is a very potent contributor to the inflammation of the lung airways (bronchial tubes) in allergic asthma.