Page 956 - Veterinary Immunology, 10th Edition

Eosinophil Activation, 332
VetBooks.ir Eosinophil Degranulation and Mediators,

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LEARNING OBJECTIVES

After reading this chapter, you should be able to:

• Describe the structure, location and properties of mast cells, eosinophils, and
basophils.
• Explain how type I hypersensitivities result from type 2 immune responses

mediated by immunoglobulin E (IgE).
• Describe how mast cells respond to the binding of antigen to cell bound IgE.
• Describe the structure and properties of IgE.

• Discuss how allergic disease is caused by the release of inflammatory molecules
from mast cells, eosinophils, and basophils.
• List the major inflammatory molecules released by each of these cells.

• Describe the ways in which mast cell responses are regulated.
• Understand how these responses probably evolved as a specialized defensive
response against parasitic helminths and arthropods.

• Describe the pathways involved in the mobilization of eosinophils.
• Explain how these types of response are affected by the composition of the

intestinal microbiota.

Pathologic lesions triggered by immune responses are called
hypersensitivities. They are classified into four major types based
on their pathogenic mechanisms. Type I hypersensitivity reactions
are inflammatory responses that result from the release of the
contents of mast cell, basophil, and eosinophil cytoplasmic

granules. This granule release is triggered when antigens bind to
immunoglobulin E (IgE) on the surface of mast cells or basophils.
These granules contain a mixture of molecules that trigger

inflammation and attract eosinophils (Fig. 29.1). This inflammation

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