Th1- and Th2-type cytokines regulate chemokine expression.
The recruitment of various leukocyte populations to an area of injured and inflamed tissue is one of the most fundamental host defense responses. Historic evidence supports the concept that the pathology of acute inflammation is characterized by the elicitation of neutrophils, while the leukocyte composition of more chronic inflammatory responses is mononuclear in nature. Interestingly, little is known regarding the mechanism involved in the "switch' from an acute neutrophil-mediated response to a chronic mononuclear-cell-directed immune reaction. Recent studies demonstrate that two supergene families of chemokines play a key role in dictating the recruitment of specific leukocyte populations necessary for the appropriate inflammatory response. The expression of specific chemokines appears to be under the control of other cytokines, such as interleukins-1, -4 and -10, and tumor necrosis factor, that serve as either positive or negative regulatory mediators in the control of chemokine production, thus, controlling the recruitment of leukocyte subpopulations.
Department of Pathology, University of Michigan Medical School, Ann Arbor, USA.
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Kunkel
D018932:Chemokine CCL2 / Q000096:biosynthesis; D018925:Chemokines / Q000096:biosynthesis*; D004797:Enzyme-Linked Immunosorbent Assay; D006801:Humans; D007371:Interferon-gamma / Q000494:pharmacology; D007375:Interleukin-1 / Q000494:pharmacology; D016753:Interleukin-10; D008070:Lipopolysaccharides / Q000494:pharmacology; D018417:Th1 Cells / Q000187:drug effects / Q000502:physiology*; D018418:Th2 Cells / Q000187:drug effects / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
D018932:Chemokine CCL2; D018925:Chemokines; D007375:Interleukin-1; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D007371:Interferon-gamma