The molecular understanding of leukocyte recruitment and migration has provided a large number of potential therapeutic targets for controlling harmful inflammation. Agents that block TNF, one of the major cytokines in leukocyte recruitment, are among the most successful therapeutics ever developed for chronic inflammatory diseases, and antagonists of leukocyte integrins are approved for inflammatory diseases and are being tested in clinical trials. Predictably, these antagonists not only have the desired effect of controlling the inflammation but can also compromise the ability of treated patients to defend themselves against microbes, which, of course, is the physiologic function of the inflammatory response.
Leukocytes are recruited from the blood into the extravascular tissue where infectious pathogens or damaged tissues may be located, migrate to the site of infection or tissue injury, and are activated to perform their functions.
Leukocyte recruitment is a multistep process consisting of loose attachment to and rolling on endothelium (mediated by selectins); firm attachment to endothelium (mediated by integrins); and migration through interendothelial gaps.
Various cytokines promote the expression of selectins and integrin ligands on endothelium (TNF, IL-1), increase the avidity of integrins for their ligands (chemokines), and promote directional migration of leukocytes (also chemokines).Tissue macrophages and other cells responding to the pathogens or damaged tissues produce many of these cytokines.
Neutrophils predominate in the early inflammatory infiltrate and are later replaced by monocytes and macrophages.
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Fig. 3.5 Nature of leukocyte infiltrates in inflammatory reactions. The photomicrographs show an inflammatory reaction in the myocardium after ischemic necrosis (infarction). (A) Early (neutrophilic) infiltrates and congested blood vessels. (B) Later (mononuclear) cellular infiltrates. (C) The approximate kinetics of edema and cellular infiltration. For simplicity, edema is shown as an acute transient response, although secondary waves of delayed edema and neutrophil infiltration also can occur.
Phagocytosis and Clearance of of infection or tissue injury they must be activated to perform their functions. This makes perfect sense because, the Offending Agent while we want our defenders to patrol our body constantly, Recognition of microbes or dead cells induces several it would be wasteful to keep them at a high level of alert responses in leukocytes that are collectively called leuko-and expending energy before they are required. The funccyte activation (
Fig. 3.6 ). After leukocytes (particularly tional responses that are most important for destruction  neutrophils and monocytes) have been recruited to a site of microbes and other offenders are phagocytosis and
A 1. RECOGNITION AND ATTACHMENT Microbes bind to phagocyte receptors
Degradation of microbes 2. ENGULFMENT by lysosomal enzymes Phagocyte membrane in phagolysosome 3. KILLING AND DEGRADATION