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Arrest, Migration, Survival and Proliferation of Leukocytes and Vascular Cells: The Many Faces of Chemokine Biology
Author(s) -
LEY KLAUS
Publication year - 2003
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1038/sj.mn.7800189
Subject(s) - citation , chemokine , library science , medicine , immunology , computer science , inflammation
This issue of Microcirculation explores the role of chemokines, a family of small, secreted peptides that regulate leukocyte traffic in health and disease. Leading experts review the diverse function of these mediators, with an emphasis on their roles in microvascular physiology and pathophysiology. The most amazing aspect of this field of research is the diversity of functions that have been attributed to chemokines. Chemokines are classified according to their amino acid sequence as CC (no intervening amino acid between first two cysteinyl residues), CXC (one intervening amino acid), CX3C (three intervening amino acids), and XC (only one cysteinyl residue). They are numbered as CCL1–27, CXCL1–16, CX3CL1, and XCL1 (10,11,15). They bind to at least 11 CC receptors (CCR1–11), 6 CXC receptors (CXCR1–6), CX3CR1, and XCR1 (10,11,15). Earlier notions that CXC chemokines attract granulocytes and CC receptors are responsible for mononuclear cell effects have been supplanted by more recent findings. Chemokines may have emerged early in evolution from proteolytic fragments of tyrosyl transfer RNA synthetase, an essential intracellular enzyme, even before a circulatory system developed (15,16). In complex mammalian organisms, chemokines not only regulate leukocyte development and chemotaxis, but also play important roles in their trafficking through the vascular and lymphatic systems. Some, but not all chemokines can be immobilized on the endothelial surface and can activate integrin adhesion receptors on rolling leukocytes to promote their arrest. Two reviews in this issue (1,8) focus on the function of arrest chemokines, presenting different perspectives on how chemokine receptor signaling may be integrated with other signals in phagocytes (8) and how chemokine receptor engagement in lymphocytes will promote local integrin avidity upregulation in a fraction of a second (1). One of the first chemokines discovered was CCL2 (monocyte chemoattractant protein-1), and it may