Info

Anligan prasenLalMn IgE produclkin acîiVBlïon Modialor release Clawal ellaciis

Mucosal surface

Pharmacologic streets: blood vessels, airways, ate. ten tfihhrohan and accumulation

Clin Ici I Off«Clt: hjy fevnr asthma Outima anaphylaxis

Processing and présentation

Figure 1 Induction and effector mechanisms in type hypersensitivity. Antigen presentation is performed at the mucosal level. Production of allergen-specific IgE results from the release of TH2 cytokines from activated T cells. IgE binds to mast cells through FceR and sensitizes these cells. Allergen re-exposure cross-links surface-bound IgE and triggers Ca2 release. This leads to the production of mediators causing allergic symptoms. (Reproduced with permission from Roitt et al (1996).)

Figure 2 Lipid mediators of inflammation synthesized by mast cells upon stimulation by antigen binding to IgE. (Reproduced with permission from Janeway and Travers (1995).)

larger, harder and moderately painful. This reaction is caused by the release of PGD2 and leukotrienes by T cells and eosinophils.

RAST (radioallergosorbent test)

RAST evaluates antigen-specific IgE in the serum. This usually correlates with skin-prick tests. There is also a group of allergic patients who are both skin test- and RAST-negative. These individuals make a local antibody response and this is shown by a positive nasal or bronchial provocation test with specific antigen.

Beneficial role of IgE

If the entry of a parasite is not blocked at the level of the gut by a defensive, neutralizing IgA mechanism, the contact of this agent with IgE-sensitized mast cells and basophils will release immune mediators. The response to helminth and nematode infections is due to the induction of Tn2 cells to secrete IL-3, IL-4 and IL-5, which promote B cell and mucosal mast cell proliferation and eosinophil activation. The result is an increased IgE production and eosinophilia, which are the hallmarks of this type of immune response. Eosinophils have evolved specifically as a defense against parasites that are too large to be phagocytosed; the mast cells have evolved primarily to localize eosinophils near the parasites and to enhance their antiparasitic function. In contrast to allergy, the Igf^ response to parasites operates against a broad range of parasitic antigens. This response saturates the high-affinity receptors on mast cells, rendering them refractory to further triggering by parasites.

The effector role in host defenses is mainly performed by the eosinophils and IgE-sensitized mast cell interactions with the parasites via IgE FceRU and eBP. The consequences are: 1) release of granule con tents, including the eosinphil major basic protein which lyses the worms; 2) secretion of mucus, which creates a barrier to the attachment and invasion; and 3) increased vascular permeability and chemotaxis, which allows the penetration of complement, IgG and effector cells back into the gut, thereby enhancing the expulsion of the worms. Furthermore, production of proinflammatory cytokines by activated macrophages ultimately increases mucus secretion and facilitates the expulsion of the worms.

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