Page 1056 - Veterinary Immunology, 10th Edition

between and beneath vascular endothelial cells. Complement
VetBooks.ir components activated by the classical pathway will be deposited

here as well.
Immune complexes formed in tissues must be removed. They

first bind to Fc and complement receptors on cells. The most
widespread of these Fc receptors is FcγRIIa (CD32a) expressed on
neutrophils. Immune complexes binding to these receptors activate
the neutrophils and stimulate production of oxidants, leukotrienes,

prostaglandins, cytokines, and chemokines. Immune complexes
also bind to mast cells through FcγRIII and trigger them to release
their granule contents. Among the molecules released by mast cells
are chemoattractants and proteases that activate complement,

cytokines, kinins, and lipid mediators. All these mediators promote
inflammation by acting on vascular endothelium and stimulating
neutrophil adherence and emigration.
Immune complexes activate complement and generate the

chemotactic peptide C5a (Fig. 32.2). Neutrophils, attracted by C5a
and mast cell–derived chemokines, emigrate from the blood vessels,
adhere to the complexes, and promptly phagocytose them.
Eventually the immune complexes are digested and destroyed.

During this process, however, more proteases and oxidants are
released into the tissues. When neutrophils attempt to ingest
immune complexes attached to structures such as basement
membranes, they release their granule contents directly into the

surrounding tissues. Neutrophil proteases disrupt collagen fibers
and destroy ground substances, basement membranes, and elastic
tissue. Normally tissues contain antiproteinases that inhibit
neutrophil enzymes. However, neutrophils can subvert these
−
−
inhibitors by secreting OCl . The OCl destroys the inhibitors and
allows tissue destruction to proceed.

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