Chemokines inInnate andAdaptiveHostDefense: Basic Chemokinese Grammar for Immune Cells

Abstract

Chemokines compose a sophisticated communication system used by all our cell types, including immune cells. Chemokine messages are decoded by specific receptors that initiate signal transduction events leading to a multitude of cellular responses, leukocyte chemotaxis and adhesion in particular. Critical determinants of the in vivo activities of chemokines in the immune system include their presentation by endothelial cells and extracellular matrix molecules, as well as their cellular uptake via "silent" chemokine receptors (interceptors) leading either to their transcytosis or to degradation. These regulatory mechanisms of chemokine histotopography, as well as the promiscuous and overlapping receptor specificities of inflammation-induced chemokines, shape innate responses to infections and tissue damage. Conversely, the specific patterns of homeostatic chemokines, where each chemokine is perceived by a single receptor, are charting lymphocyte navigation routes for immune surveillance. This review presents our current understanding of the mechanisms that regulate the cellular perception and pathophysiologic meaning of chemokines.

Basic chemokine-derived glycosaminoglycan binding peptides exert antiviral properties against dengue virus serotype 2, herpes simplex virus-1 and respiratory syncytial virus

“…Chemokines are a class of leukocyte chemotactic cytokines which exert their function through binding both to GAGs and to G protein-coupled receptors (GPCRs) and GAG binding is indispensable for the in vivo function of chemokines [35][36][37][38][39][40][41][42]. Chemokines can be divided into four groups based on the position of two conserved NH2-terminal cysteine residues.…”

CCR6 regulates EAE pathogenesis by controlling regulatory CD4+ T‐cell recruitment to target tissues

“…Differentiation is accompanied by sequential expression of selectins, integrins, and chemokine receptors responsible for T-cell-subset recruitment to and extravasation at inflammation sites. The correct in vivo location of these cell subsets, necessary for their interaction with accessory or target cells, is regulated by chemokines and their receptors [11], which are assumed to have a critical impact on MS and EAE pathogenesis [12].…”

Monocyte and neutrophil recruitment during oral Salmonella infection is driven by MyD88‐derived chemokines

“…Despite the undisputed role of chemokine receptors and their ligands in ensuring survival to infection, it is difficult to assess the role of individual chemokines in phagocyte recruitment, particularly in the complex environment of bacterial-infected tissues. For instance, different infection models can induce distinct chemokine profiles, most chemokine receptors are bound by multiple ligands and chemokine receptor/ligand pairs have overlapping roles [17,18]. Moreover, although chemokine-deficient models have shown increased bacterial burden during Salmonella infection, [19][20][21], it is not known which chemokines are induced in the intestinal lymphoid tissue during oral Salmonella infection or where and by what cells the chemokines are produced.…”