Abstract
The process of inflammation and immune recognition involve a complex series of events that result in an accumulation of specific leukocyte subsets at the site of tissue alteration or damage. These processes involve activation of cellular components and release of reactive mediators, changes in vascular endothelium, and penetration of the basement membrane, as well as chemotaxis of specific leukocyte subsets to the site of injury and infiltration into the tissue site (1–4). While these extravasating leukocytes are critical for host defense, leading to clearance of the inciting factors such as infectious agents, it should also be appreciated that leukocyte recruitment may also contribute to the pathogenesis of an underlying disease. The maintenance of leukocyte recruitment during inflammation requires a “delicate” communication between infiltrating leukocytes and the endothelium (1–5). These signals are mediated via the generation of several early response cytokines (such as interleukin-1 [IL-1] and tumor necrosis factor-α [TNF-α]), the expression of surface adhesion molecules, and the production of chemotactic molecules. All these processes, in one way or another, have been shown to be involved in the localization of neutrophils, monocytes, macrophages, eosinophils, basophils, T- and B-lymphocytes, and natural killer (NK) cells to inflammatory sites. In many disease states, this recruitment appears to be selective in that neutrophils are typically present in sites of acute inflammation whereas macrophages and lymphocytes are typically present at sites of chronic inflammation or at the later stages of disease. Likewise, in viral infections (6, 7) and during the rejection of allografts (8), NK cells selectively accumulate in the inflammatory site, in many cases before T-cell infiltration.
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Taub, D.D. (1999). Natural Killer Cell-Chemokine Interactions. In: Rollins, B.J. (eds) Chemokines and Cancer. Contemporary Cancer Research. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-59259-701-7_5
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