Page 940 - Veterinary Immunology, 10th Edition
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FIG. 28.9 The mechanisms involved in the self-cure reaction
against intestinal helminths. In essence, the animal mounts an
allergic response to the salivary antigens of attached nematodes.
This acute inflammatory response causes the worms to detach from
the intestinal wall and pass out in the feces.
Mast cells are also required for helminth expulsion. Mast cell
numbers increase in the tissues during helminth infection. They can
also be activated directly by PAMPs through PRRs, although it is
unclear which parasite PAMPs do this. In response, these mast cells
produce IL-4, -13, and -5, plus chemotactic factors. Mast cell
proteases degrade tight junctions and allow fluid efflux into the
intestine. Mast cell products may be directly toxic to helminths.
Basophils are also attracted to attached worms and are a major
source of IL-4. Basophils can act as antigen-presenting cells in
helminth (Trichuris muris) infections.
The combination of helminth antigens with mast cell–bound IgE
triggers mast cell degranulation and the release of vasoactive
amines such as histamine, cytokines such as IL-13 and IL-33,
chitinases, and proteases. These molecules stimulate vigorous
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