Journal articles: 'Chemokines'

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Struyf, Sofie, Paul Proost, Jean-Pierre Lenaerts, Griet Stoops, Anja Wuyts, and Jo Van Damme. "Identification of a blood-derived chemoattractant for neutrophils and lymphocytes as a novel CC chemokine, Regakine-1." Blood 97, no. 8 (April 15, 2001): 2197–204. http://dx.doi.org/10.1182/blood.v97.8.2197.

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Abstract Chemokines constitute a large family of chemotactic cytokines that selectively attract different blood cell types. Although most inflammatory chemoattractants are only induced and released in the circulation during acute infection, a restricted number of CXC and CC chemokines are constitutively present in normal plasma at high concentrations. Here, such a chemotactic protein was purified to homogeneity from serum and fully identified as a novel CC chemokine by mass spectrometry and amino acid sequence analysis. The protein, tentatively designated Regakine-1, shows less than 50% sequence identity with any known chemokine. This novel CC chemokine chemoattracts both neutrophils and lymphocytes but not monocytes or eosinophils. Its modest chemotactic potency but high blood concentration is similar to that of other chemokines present in the circulation, such as hemofiltrate CC chemokine-1, platelet factor-4, and β-thromboglobulin. Regakine-1 did not induce neutrophil chemokinesis. However, it synergized with the CXC chemokines interleukin-8 and granulocyte chemotactic protein-2, and the CC chemokine monocyte chemotactic protein-3, resulting in an at least a 2-fold increase of the neutrophil and lymphocyte chemotactic response, respectively. The biologic effects of homogeneous natural Regakine-1 were confirmed with chemically synthesized chemokine. Like other plasma chemokines, it is expected that Regakine-1 plays a unique role in the circulation during normal or pathologic conditions.

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Palomino, Diana Carolina Torres, and Luciana Cavalheiro Marti. "Chemokines and immunity." Einstein (São Paulo) 13, no. 3 (September 2015): 469–73. http://dx.doi.org/10.1590/s1679-45082015rb3438.

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Chemokines are a large family of small cytokines and generally have low molecular weight ranging from 7 to 15kDa. Chemokines and their receptors are able to control the migration and residence of all immune cells. Some chemokines are considered pro-inflammatory, and their release can be induced during an immune response at a site of infection, while others are considered homeostatic and are involved in controlling of cells migration during tissue development or maintenance. The physiologic importance of this family of mediators is resulting from their specificity − members of the chemokine family induce recruitment of well-defined leukocyte subsets. There are two major chemokine sub-families based upon cysteine residues position: CXC and CC. As a general rule, members of the CXC chemokines are chemotactic for neutrophils, and CC chemokines are chemotactic for monocytes and sub-set of lymphocytes, although there are some exceptions. This review discusses the potential role of chemokines in inflammation focusing on the two best-characterized chemokines: monocyte chemoattractant protein-1, a CC chemokine, and interleukin-8, a member of the CXC chemokine sub-family.

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Parry, Christopher M., J. Pedro Simas, Vincent P. Smith, C. Andrew Stewart, Anthony C. Minson, Stacey Efstathiou, and Antonio Alcami. "A Broad Spectrum Secreted Chemokine Binding Protein Encoded by a Herpesvirus." Journal of Experimental Medicine 191, no. 3 (February 7, 2000): 573–78. http://dx.doi.org/10.1084/jem.191.3.573.

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Chemokines are a family of small proteins that interact with seven-transmembrane domain receptors and modulate the migration of immune cells into sites of inflammation and infection. The murine gammaherpesvirus 68 M3 gene encodes a secreted 44-kD protein with no sequence similarity to known chemokine receptors. We show that M3 binds a broad range of chemokines, including CC, CXC, C, and CX3C chemokines, but does not bind human B cell–specific nor mouse neutrophil–specific CXC chemokines. This herpesvirus chemokine binding protein (hvCKBP) blocks the interaction of chemokines with high-affinity cellular receptors and inhibits chemokine-induced elevation of intracellular calcium levels. hvCKBP is the first soluble chemokine receptor identified in herpesviruses; it represents a novel protein structure with the ability to bind all subfamilies of chemokines in solution and has potential therapeutic applications.

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Palacios-Arreola, M. Isabel, Karen E. Nava-Castro, Julieta I. Castro, Eduardo García-Zepeda, Julio C. Carrero, and Jorge Morales-Montor. "The Role of Chemokines in Breast Cancer Pathology and Its Possible Use as Therapeutic Targets." Journal of Immunology Research 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/849720.

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Chemokines are small proteins that primarily regulate the traffic of leukocytes under homeostatic conditions and during specific immune responses. The chemokine-chemokine receptor system comprises almost 50 chemokines and approximately 20 chemokine receptors; thus, there is no unique ligand for each receptor and the binding of different chemokines to the same receptor might have disparate effects. Complicating the system further, these effects depend on the cellular milieu. In cancer, although chemokines are associated primarily with the generation of a protumoral microenvironment and organ-directed metastasis, they also mediate other phenomena related to disease progression, such as angiogenesis and even chemoresistance. Therefore, the chemokine system is becoming a target in cancer therapeutics. We review the emerging data and correlations between chemokines/chemokine receptors and breast cancer, their implications in cancer progression, and possible therapeutic strategies that exploit the chemokine system.

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Dyer, Douglas P., Elisa Migliorini, Catherina L. Salanga, Dhruv Thakar, Tracy M. Handel, and Ralf P. Richter. "Differential structural remodelling of heparan sulfate by chemokines: the role of chemokine oligomerization." Open Biology 7, no. 1 (January 2017): 160286. http://dx.doi.org/10.1098/rsob.160286.

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Chemokines control the migration of cells in normal physiological processes and in the context of disease such as inflammation, autoimmunity and cancer. Two major interactions are involved: (i) binding of chemokines to chemokine receptors, which activates the cellular machinery required for movement; and (ii) binding of chemokines to glycosaminoglycans (GAGs), which facilitates the organization of chemokines into haptotactic gradients that direct cell movement. Chemokines can bind and activate their receptors as monomers; however, the ability to oligomerize is critical for the function of many chemokines in vivo . Chemokine oligomerization is thought to enhance their affinity for GAGs, and here we show that it significantly affects the ability of chemokines to accumulate on and be retained by heparan sulfate (HS). We also demonstrate that several chemokines differentially rigidify and cross-link HS, thereby affecting HS rigidity and mobility, and that HS cross-linking is significantly enhanced by chemokine oligomerization. These findings suggest that chemokine–GAG interactions may play more diverse biological roles than the traditional paradigms of physical immobilization and establishment of chemokine gradients; we hypothesize that they may promote receptor-independent events such as physical re-organization of the endothelial glycocalyx and extracellular matrix, as well as signalling through proteoglycans to facilitate leukocyte adhesion and transmigration.

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Horuk, Richard. "Chemokines." Scientific World JOURNAL 7 (2007): 224–32. http://dx.doi.org/10.1100/tsw.2007.6.

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Chemokines are a family of polypeptides that direct the migration of leukocytestoward a site of infection. They play a major role in autoimmune disease and chemokine receptors have recently been found to mediate HIV-1 fusion. In this short review we examine the role of chemokines in host defence and in the pathophysiology of autoimmune diseases. We conclude by discussing various therapeutic approaches that target chemokine receptors and that could be beneficial in disease.

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Blanchet, Xavier, Christian Weber, and Philipp von Hundelshausen. "Chemokine Heteromers and Their Impact on Cellular Function—A Conceptual Framework." International Journal of Molecular Sciences 24, no. 13 (June 30, 2023): 10925. http://dx.doi.org/10.3390/ijms241310925.

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Chemoattractant cytokines or chemokines are proteins involved in numerous biological activities. Their essential role consists of the formation of gradient and (immune) cell recruitment. Chemokine biology and its related signaling system is more complex than simple ligand–receptor interactions. Beside interactions with their cognate and/or atypical chemokine receptors, and glycosaminoglycans (GAGs), chemokines form complexes with themselves as homo-oligomers, heteromers and also with other soluble effector proteins, including the atypical chemokine MIF, carbohydrate-binding proteins (galectins), damage-associated molecular patterns (DAMPs) or with chemokine-binding proteins such as evasins. Likewise, nucleic acids have been described as binding targets for the tetrameric form of CXCL4. The dynamic balance between monomeric and dimeric structures, as well as interactions with GAGs, modulate the concentrations of free chemokines available along with the nature of the gradient. Dimerization of chemokines changes the canonical monomeric fold into two main dimeric structures, namely CC- and CXC-type dimers. Recent studies highlighted that chemokine dimer formation is a frequent event that could occur under pathophysiological conditions. The structural changes dictated by chemokine dimerization confer additional biological activities, e.g., biased signaling. The present review will provide a short overview of the known functionality of chemokines together with the consequences of the interactions engaged by the chemokines with other proteins. Finally, we will present potential therapeutic tools targeting the chemokine multimeric structures that could modulate their biological functions.

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Mackay, Charles R. "Chemokines: What chemokine is that?" Current Biology 7, no. 6 (June 1997): R384—R386. http://dx.doi.org/10.1016/s0960-9822(06)00181-3.

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9

ABBADIE, C. "Chemokines, chemokine receptors and pain." Trends in Immunology 26, no. 10 (October 2005): 529–34. http://dx.doi.org/10.1016/j.it.2005.08.001.

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Kaplan, Allen P. "Chemokines, Chemokine Receptors and Allergy." International Archives of Allergy and Immunology 124, no. 4 (2001): 423–31. http://dx.doi.org/10.1159/000053777.

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Youn, Byung-S., Charlie Mantel, and Hal E. Broxmeyer1. "Chemokines, chemokine receptors and hematopoiesis." Immunological Reviews 177, no. 1 (October 2000): 150–74. http://dx.doi.org/10.1034/j.1600-065x.2000.17701.x.

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Colditz, Ian, Martin Schneider, Monika Pruenster, and Antal Rot. "Chemokines at large: In-vivo mechanisms of their transport, presentation and clearance." Thrombosis and Haemostasis 97, no. 05 (2007): 688–93. http://dx.doi.org/10.1160/th07-02-0105.

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SummaryCompelling evidence implicates chemokines in the induction of leukocyte emigration from blood into tissues.This arguably most fundamental effect of chemokines is accomplished by triggering cognate classical G-protein-coupled chemokine receptors on the leukocyte surface. In vitro, these same receptors mediate leukocyte migration; however, the mechanisms of chemokine-induced migration differ between in-vivo and in-vitro settings. Leukocyte egress from blood is greatly influenced by haemodynamic conditions and requires full cooperation of endothelial cells.The behaviour of chemokines in their“native habitat” in vivo is controlled by their interaction with several accessory molecules which influence immobilisation, transport, clearance and degradation of chemokines and thereby determine the sites and duration of their action. Here we discuss peculiarities of the invivo actions of chemokines,the mechanisms of chemokine interaction with receptors and auxiliary molecules including interceptors, glycosaminoglycans and enzymes and illustrate how these interactions influence the outcome of chemokine activities in vivo.

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WARD, Stephen G., and John WESTWICK. "Chemokines: understanding their role in T-lymphocyte biology." Biochemical Journal 333, no. 3 (August 1, 1998): 457–70. http://dx.doi.org/10.1042/bj3330457.

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The chemokines are a complex superfamily of small, secreted proteins that were initially characterized through their chemotactic effects on a variety of leucocytes. The superfamily is divided into families based on structural and genetic considerations and have been termed the CXC, CC, C and CX3C families. Chemokines from these families have a key role in the recruitment and function of T lymphocytes. Moreover, T lymphocytes have also been identified as a source of a number of chemokines. T lymphocytes also express most of the known CXC and CC chemokine receptors to an extent that depends on their state of activation/differentiation and/or the activating stimuli. The expression of two chemokine receptors, namely CXCR4 and CCR5, together with the regulated production of their respective ligands, appears to be extremely important in determining sensitivity of T cells to HIV-1 infection. The intracellular events which mediate the effects of chemokines, particularly those elicited by the CC chemokine RANTES, include activation of both G-protein- and protein tyrosine kinase-coupled signalling pathways. The present review describes our current understanding of the structure and expression of chemokines and their receptors, the effects of chemokines on T-cell function(s), the intracellular signalling pathways activated by chemokines and the role of certain chemokines and chemokine receptors in determining sensitivity to HIV-1 infection.

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Weber, Michele, Emma Blair, Clare V. Simpson, Maureen O'Hara, Paul E. Blackburn, Antal Rot, Gerard J. Graham, and Robert J. B. Nibbs. "The Chemokine Receptor D6 Constitutively Traffics to and from the Cell Surface to Internalize and Degrade Chemokines." Molecular Biology of the Cell 15, no. 5 (May 2004): 2492–508. http://dx.doi.org/10.1091/mbc.e03-09-0634.

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The D6 heptahelical membrane protein, expressed by lymphatic endothelial cells, is able to bind with high affinity to multiple proinflammatory CC chemokines. However, this binding does not allow D6 to couple to the signaling pathways activated by typical chemokine receptors such as CC-chemokine receptor-5 (CCR5). Here, we show that D6, like CCR5, can rapidly internalize chemokines. However, D6-internalized chemokines are more effectively retained intracellularly because they more readily dissociate from the receptor during vesicle acidification. These chemokines are then degraded while the receptor recycles to the cell surface. Interestingly, D6-mediated chemokine internalization occurs without bringing about a reduction in cell surface D6 levels. This is possible because unlike CCR5, D6 is predominantly localized in recycling endosomes capable of trafficking to and from the cell surface in the absence of ligand. When chemokine is present, it can enter the cells associated with D6 already destined for internalization. By this mechanism, D6 can target chemokines for degradation without the necessity for cell signaling, and without desensitizing the cell to subsequent chemokine exposure.

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Pruenster, M., and A. Rot. "Throwing light on DARC." Biochemical Society Transactions 34, no. 6 (October 25, 2006): 1005–8. http://dx.doi.org/10.1042/bst0341005.

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Chemokines play a key role in directing and driving leucocyte trafficking. The efficient regulation of leucocyte recruitment by chemokines requires their appropriate localization in functional micro-anatomical domains, as well as setting limits to their effects in space and time. Both processes are influenced by silent chemokine receptors (interceptors), including DARC (Duffy antigen receptor for chemokines). Increasing experimental evidence suggests that DARC is involved in accumulation of extravascular chemokines in endothelial cells, chemokine transcytosis and presentation on their luminal surface, leading to leucocyte adhesion and emigration. Additionally, DARC is expressed on erythrocytes and can act as a sink for chemokines in blood. This limits the dissemination of chemokines through blood into distant organs and tissues as well as reducing their effects on the circulating leucocytes.

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Schwartzkopff, Franziska, Frank Petersen, Tobias Alexander Grimm, and Ernst Brandt. "CXC chemokine ligand 4 (CXCL4) down-regulates CC chemokine receptor expression on human monocytes." Innate Immunity 18, no. 1 (November 18, 2010): 124–39. http://dx.doi.org/10.1177/1753425910388833.

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During acute inflammation, monocytes are essential in abolishing invading micro-organisms and encouraging wound healing. Recruitment by CC chemokines is an important step in targeting monocytes to the inflamed tissue. However, cell surface expression of the corresponding chemokine receptors is subject to regulation by various endogenous stimuli which so far have not been comprehensively identified. We report that the platelet-derived CXC chemokine ligand 4 (CXCL4), a known activator of human monocytes, induces down-regulation of CC chemokine receptors (CCR) 1, −2, and −5, resulting in drastic impairment of monocyte chemotactic migration towards cognate CC chemokine ligands (CCL) for these receptors. Interestingly, CXCL4-mediated down-regulation of CCR1, CCR2 and CCR5 was strongly dependent on the chemokine’s ability to stimulate autocrine/paracrine release of TNF-α. In turn, TNF-α induced the secretion CCL3 and CCL4, two chemokines selective for CCR1 and CCR5, while the secretion of CCR2-ligand CCL2 was TNF-α-independent. Culture supernatants of CXCL4-stimulated monocytes as well as chemokine-enriched preparations thereof reproduced CXCL4-induced CCR down-regulation. In conclusion, CXCL4 may act as a selective regulator of monocyte migration by stimulating the release of autocrine, receptor-desensitizing chemokine ligands. Our results stress a co-ordinating role for CXCL4 in the cross-talk between platelets and monocytes during early inflammation.

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Alcamí, Antonio, Julian A. Symons, Paul D. Collins, Timothy J. Williams, and Geoffrey L. Smith. "Blockade of Chemokine Activity by a Soluble Chemokine Binding Protein from Vaccinia Virus." Journal of Immunology 160, no. 2 (January 15, 1998): 624–33. http://dx.doi.org/10.4049/jimmunol.160.2.624.

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Abstract Chemokines direct migration of immune cells into sites of inflammation and infection. Chemokine receptors are seven-transmembrane domain proteins that, in contrast to other cytokine receptors, cannot be easily engineered as soluble chemokine inhibitors. Poxviruses encode several soluble cytokine receptors to evade immune surveillance, providing new strategies for immune modulation. Here we show that vaccinia virus and other orthopoxviruses (cowpox and camelpox) express a secreted 35-kDa chemokine binding protein (vCKBP) with no sequence similarity to known cellular chemokine receptors. The vCKBP binds CC, but not CXC or C, chemokines with high affinity (Kd = 0.1–15 nM for different CC chemokines), blocks the interaction of chemokines with cellular receptors, and inhibits chemokine-induced elevation of intracellular calcium levels and cell migration in vitro, thus representing a soluble inhibitor that binds and sequesters chemokines. The potential of vCKBP as a therapeutic agent in vivo was illustrated in a guinea pig skin model by the blockade of eotaxin-induced eosinophil infiltration, a feature of allergic inflammatory reactions. Furthermore, vCKBP may enable the rational design of antagonists to neutralize pathogens that use chemokine receptors to initiate infection, such as HIV or the malarial parasite.

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Groves, D. T., and Y. Jiang. "Chemokines, a Family of Chemotactic Cytokines." Critical Reviews in Oral Biology & Medicine 6, no. 2 (April 1995): 109–18. http://dx.doi.org/10.1177/10454411950060020101.

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Chemokines are low-molecular-weight proteins that stimulate recruitment of leukocytes. They are secondary proinflammatory mediators that are induced by primary pro-inflammatory mediators such as interleukin-I (IL-1) or tumor necrosis factor (TNF). The physiologic importance of this family of mediators is derived from their specificity. Unlike the classic leukocyte chemo-attractants, which have little specificity, members of the chemokine family induce recruitment of well-defined leukocyte subsets. Thus, chemokine expression can account for the presence of different types of leukocytes observed in various normal or pathologic states. There are two major chemokine sub-families based upon the position of cysteine residues, i . e.,CXC and CC. All members of the CXC chemokine sub-family have an intervening amino acid between the first two cysteines; members of the CC chemokine sub-family have two adjacent cysteines. As a general rule (with some notable exceptions), members of the CXC chemokines are chemotactic for neutrophils, and CC chemokines are chemotactic for monocytes and a small sub-set of lymphocytes. This review discusses the potential role of chemokines in inflammation and focuses on the two best-characterized chemokines, monocyte chemoattractant protein-1 (MCP-1 a CC chemokine, and interleukin-8 (IL-8), a member of the CXC chemokine sub-family.

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Maghazachi, A. A., A. al-Aoukaty, and T. J. Schall. "C-C chemokines induce the chemotaxis of NK and IL-2-activated NK cells. Role for G proteins." Journal of Immunology 153, no. 11 (December 1, 1994): 4969–77. http://dx.doi.org/10.4049/jimmunol.153.11.4969.

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Abstract The C-C chemokines MIP-1 alpha, MCP-1, and RANTES, but not MIP-1 beta, induce the chemotaxis of NK and IL-2-activated NK (IANK) cells, as determined in microchemotaxis assay. Only RANTES and MCP-1, but not MIP-1 alpha were able to induce the chemokinesis of NK cells. In contrast, none of the C-C chemokines tested was able to induce the chemokinesis of IANK cells. IANK cell chemotaxis in response to MCP-1 or RANTES but not MIP-1 alpha, was inhibited by pertussis toxin (PT). In contrast, cholera toxin (CT) inhibited the ability of all three chemokines to induce the chemotaxis of IANK cells. IANK cells intoxicated with PT lost their ability to migrate in response to RANTES and MCP-1 but not MIP-1 alpha, whereas those intoxicated with CT lost their ability to migrate in response to the three C-C chemokines tested. These results suggest that guanine nucleotide binding (G) proteins are coupled to C-C chemokine receptors in IANK cells. Subsequently, we observed that MIP-1 alpha, MCP-1, and RANTES, but not MIP-1 beta, enhance the binding of guanosine 5'-O-(thiotriphosphate), and increase the hydrolysis of [32P]GTP in IANK cell membranes. Further analysis showed that MIP-1 alpha, RANTES, or MCP-1 did not enhance GTP binding in membranes prepared from IANK cells intoxicated with CT, whereas only RANTES and MCP-1 but not MIP-1 alpha lost their ability to enhance GTP binding to IANK cell membranes prepared from PT-intoxicated cells. The differential inhibitory activity of CT and PT suggests that C-C chemokine receptors are coupled to different G proteins in IANK cells.

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Middleton, Jim, Angela M. Patterson, Lucy Gardner, Caroline Schmutz, and Brian A. Ashton. "Leukocyte extravasation: chemokine transport and presentation by the endothelium." Blood 100, no. 12 (December 1, 2002): 3853–60. http://dx.doi.org/10.1182/blood.v100.12.3853.

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At sites of inflammation and in normal immune surveillance, chemokines direct leukocyte migration across the endothelium. Many cell types that are extravascular can produce chemokines, and for these mediators to directly elicit leukocyte migration from the blood, they would need to reach the luminal surface of the endothelium. This article reviews the evidence that endothelial cells are active in transcytosing chemokines to their luminal surfaces, where they are presented to leukocytes. The endothelial binding sites that transport and present chemokines include glycosaminoglycans (GAGs) and possibly the Duffy antigen/receptor for chemokines (DARC). The binding residues on chemokines that interact with GAGs are discussed, as are the carbohydrate structures on GAGs that bind these cytokines. The expression of particular GAG structures by endothelial cells may lend selectivity to the type of chemokine presented in a given tissue, thereby contributing to selective leukocyte recruitment. At the luminal surface of the endothelium, chemokines are preferentially presented to blood leukocytes on the tips of microvillous processes. Similarly, certain adhesion molecules and chemokine receptors are also preferentially distributed on leukocyte and endothelial microvilli, and evidence suggests an important role for these structures in creating the necessary surface topography for leukocyte migration. Finally, the mechanisms of chemokine transcytosis and presentation by endothelial cells are incorporated into the current model of chemokine-driven leukocyte extravasation.

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Paoletti, Samantha, Vibor Petkovic, Silvia Sebastiani, M. Gabriela Danelon, Mariagrazia Uguccioni, and Basil O. Gerber. "A rich chemokine environment strongly enhances leukocyte migration and activities." Blood 105, no. 9 (May 1, 2005): 3405–12. http://dx.doi.org/10.1182/blood-2004-04-1648.

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AbstractThe migration of leukocytes in immune surveillance and inflammation is largely determined by their response to chemokines. While the chemokine specificities and expression patterns of chemokine receptors are well defined, it is still a matter of debate how leukocytes integrate the messages provided by different chemokines that are concomitantly produced in physiologic or pathologic situations in vivo. We present evidence for a novel regulatory mechanism of leukocyte trafficking. Our data are consistent with a mode of action where CC-chemokine receptor 7 (CCR7) agonists and unrelated, nonagonist chemokines first form a heteromeric complex, in the presence of which the triggering of CCR7 can occur at a much lower agonist concentration. The increase is synergistic and can be evoked by many but not all chemokines. Chemokine-induced synergism might provide an amplification system in “chemokine-rich” tissues, rendering leukocytes more competent to respond to migratory cues.

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Pontejo, Sergio, and Philip Murphy. "Chemokines and anionic phospholipids: new binding partners for microbial killing and apoptotic cell clearance." Journal of Immunology 208, no. 1_Supplement (May 1, 2022): 46.05. http://dx.doi.org/10.4049/jimmunol.208.supp.46.05.

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Abstract Chemokines constitute a large family of small cytokines that regulate leukocyte migration in immunity and inflammation, some of which also have direct bacteria-killing properties. While the molecular mechanism by which chemokines kill bacteria remains poorly understood, chemokines mediate cell migration by interacting with cell surface glycosaminoglycans (GAGs) and G protein-coupled receptors (GPCRs). We have discovered that many chemokines interact with high affinity with anionic membrane phospholipids, including phosphatidylserine (PS) and cardiolipin (CL) which are selectively exposed on the membrane of apoptotic cells and apoptotic extracellular vesicles (ApoEV), and bacteria, respectively. This adds to GPCRs and GAGs a third class of cell surface binding site for chemokines and expands the scope of chemokine action to the biological niches occupied by PS and CL. For instance, we found that ApoEV induce phagocyte migration for apoptotic cell clearance by presenting PS-binding chemokines on the vesicle surface to GPCRs expressed by phagocytes. This is a novel PS-dependent mechanism for chemokine delivery by extracellular vesicles potentially relevant to other areas of immunology and indicates that chemokines may play a more prominent role in the removal of dying cells than previously reported. On the other hand, we discovered that only CL-binding chemokines are antimicrobial and that CL-deficient bacteria are resistant to chemokine treatment, indicating that chemokines kill bacteria by targeting CL on the bacterial membrane. In short, we have identified chemokines as the first family of soluble cytokines whose bioactivities can be regulated by direct interaction with membrane phospholipids. Supported by NIAID/NIH intramural research program

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Svirshchevskaya, Elena V., Mariya V. Konovalova, Eugene V. Snezhkov, Rimma A. Poltavtseva, and Sergey B. Akopov. "Chemokine Homeostasis in Healthy Volunteers and during Pancreatic and Colorectal Tumor Growth in Murine Models." Current Issues in Molecular Biology 44, no. 10 (October 18, 2022): 4987–99. http://dx.doi.org/10.3390/cimb44100339.

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Chemokines are involved in the humoral regulation of body homeostasis. Changes in the blood level of chemokines were found in cancer, atherosclerosis, diabetes, and other systemic diseases. It is essential to distinguish the effects of co-morbid pathologies and cancer on the level of chemokines in the blood. We aimed to analyze, by multiplex cytometry, the levels of chemokines in the blood of healthy young volunteers as well as of intact mice and mice with CT26 colon and Pan02 pancreatic tumors. Two types of chemokines were identified both in human and murine plasmas: homeostatic ones, which were found in high concentrations (>100 pg/mL), and inducible ones, which can be undetectable or determined at very low levels (0–100 pg/mL). There was a high variability in the chemokine levels, both in healthy humans and mice. To analyze chemokine levels during tumor growth, C57BL/6 and BALB/c were inoculated with Pan02 or CT26 tumor cells, accordingly. The tumors significantly differed in the growth and the mortality of mice. However, the blood chemokine levels did not change in tumor-bearing mice until the very late stages. Taken collectively, blood chemokine level is highly variable and reflects in situ homeostasis. Care should be taken when considering chemokines as prognostic parameters or therapeutic targets in cancer.

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Li, Hui. "Update on the role of Chemokines and Chemokine Receptors in Liver Fibrosis." Journal of Gastrointestinal and Liver Diseases 32, no. 2 (June 22, 2023): 241–56. http://dx.doi.org/10.15403/jgld-4660.

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Chemokines play a critical role in cell migration and activation through binding to G-protein coupled cell- surface receptors with seven transmembrane domains. Chemokines are subdivided into four superfamilies including the CC, the CXC, the CX3C and the C families and the receptors of chemokines also segregate into four families including the CCR, CXCR, CX3CR and XCR families. Most chemokine receptors can bind to more than one chemokine and some chemokines also can bind to more than one receptor. There is ligand- receptor restriction during the binding of chemokines and special receptors. Interaction between chemokines and their receptors exerts a critical role in liver fibrogenesis through recruiting a variety of inflammatory cells into injured liver. The roles of chemokines including the CC, CXC and CX3C families on liver inflammation and fibrosis were described by the Wasmuth HE team ten years ago. Abundant evidence for pro-fibrotic or anti-fibrotic roles of chemokines and their receptors in liver fibrosis has been provided in the past decade. This paper is drawing on new evidence that has come up over the past 10 years, and uses that evidence to advance the understanding of chemokines‘ roles.

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Ermakov, Evgeny A., Irina A. Mednova, Anastasiia S. Boiko, Valentina N. Buneva, and Svetlana A. Ivanova. "Chemokine Dysregulation and Neuroinflammation in Schizophrenia: A Systematic Review." International Journal of Molecular Sciences 24, no. 3 (January 22, 2023): 2215. http://dx.doi.org/10.3390/ijms24032215.

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Chemokines are known to be immunoregulatory proteins involved not only in lymphocyte chemotaxis to the site of inflammation, but also in neuromodulation, neurogenesis, and neurotransmission. Multiple lines of evidence suggest a peripheral proinflammatory state and neuroinflammation in at least a third of patients with schizophrenia. Therefore, chemokines can be active players in these processes. In this systematic review, we analyzed the available data on chemokine dysregulation in schizophrenia and the association of chemokines with neuroinflammation. It has been shown that there is a genetic association of chemokine and chemokine receptor gene polymorphisms in schizophrenia. Besides, the most reliable data confirmed by the results of meta-analyses showed an increase in CXCL8/IL-8, CCL2/MCP-1, CCL4/MIP-1β, CCL11/eotaxin-1 in the blood of patients with schizophrenia. An increase in CXCL8 has been found in cerebrospinal fluid, but other chemokines have been less well studied. Increased/decreased expression of genes of chemokine and their receptors have been found in different areas of the brain and peripheral immune cells. The peripheral proinflammatory state may influence the expression of chemokines since their expression is regulated by pro- and anti-inflammatory cytokines. Mouse models have shown an association of schizophrenia with dysregulation of the CX3CL1-CX3CR1 and CXCL12-CXCR4 axes. Altogether, dysregulation in chemokine expression may contribute to neuroinflammation in schizophrenia. In conclusion, this evidence indicates the involvement of chemokines in the neurobiological processes associated with schizophrenia.

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Pontejo, Sergio M., and Philip M. Murphy. "Chemokines act as phosphatidylserine-bound “find-me” signals in apoptotic cell clearance." PLOS Biology 19, no. 5 (May 26, 2021): e3001259. http://dx.doi.org/10.1371/journal.pbio.3001259.

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Removal of apoptotic cells is essential for maintenance of tissue homeostasis. Chemotactic cues termed “find-me” signals attract phagocytes toward apoptotic cells, which selectively expose the anionic phospholipid phosphatidylserine (PS) and other “eat-me” signals to distinguish healthy from apoptotic cells for phagocytosis. Blebs released by apoptotic cells can deliver find-me signals; however, the mechanism is poorly understood. Here, we demonstrate that apoptotic blebs generated in vivo from mouse thymus attract phagocytes using endogenous chemokines bound to the bleb surface. We show that chemokine binding to apoptotic cells is mediated by PS and that high affinity binding of PS and other anionic phospholipids is a general property of many but not all chemokines. Chemokines are positively charged proteins that also bind to anionic glycosaminoglycans (GAGs) on cell surfaces for presentation to leukocyte G protein–coupled receptors (GPCRs). We found that apoptotic cells down-regulate GAGs as they up-regulate PS on the cell surface and that PS-bound chemokines, unlike GAG-bound chemokines, are able to directly activate chemokine receptors. Thus, we conclude that PS-bound chemokines may serve as find-me signals on apoptotic vesicles acting at cognate chemokine receptors on leukocytes.

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Choi, Young Bong, and John Nicholas. "Autocrine and Paracrine Promotion of Cell Survival and Virus Replication by Human Herpesvirus 8 Chemokines." Journal of Virology 82, no. 13 (April 23, 2008): 6501–13. http://dx.doi.org/10.1128/jvi.02396-07.

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ABSTRACT Human herpesvirus 8 (HHV-8), which is associated with the endothelial tumor Kaposi's sarcoma, encodes three CC/β-chemokines. These are expressed early during productive (lytic) infection and are believed to be involved in immune evasion, in addition to viral pathogenesis via induction of angiogenic cytokines. Here we report that two of the HHV-8 chemokines, CCR8 agonists vCCL-1 and vCCL-2, have direct effects on endothelial survival and virus replication. The v-chemokines stimulated virus replication when added to infected cultures exogenously, and CCR8 knockdown absent v-chemokine supplementation inhibited virus production, indicative of autocrine effects of endogenously produced vCCLs. This was verified and proreplication functions of each chemokine were demonstrated via shRNA-mediated vCCL depletion. The v-chemokines inhibited expression of lytic cycle-induced proapoptotic protein Bim, RNA interference-mediated suppression of which mimicked v-chemokine proreplication functions. Our data show for the first time that the v-chemokines have direct effects on virus biology, independently of their postulated immune evasion functions, and suggest that in vivo the v-chemokines might play direct roles in Kaposi's sarcomagenesis via paracrine prosurvival signaling.

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Xiao, Qiang, Jingyu Sun, Tina Rose, Dmitri Samovski, and Phillip Stahl. "Cytokine/chemokine secretion profiles in differentiated mouse muscle cells (P6341)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 184.32. http://dx.doi.org/10.4049/jimmunol.190.supp.184.32.

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Abstract Cytokines and Chemokines are a group of small proteins that are secreted primarily from immune cells and play essential roles in inflammation and infectious disease. Over the past decade, a great number of studies have demonstrated that some cytokines/chemokines are also secreted from adipocytes (adipokines), hepatocytes (hepatokines), and myocytes (myokines). These non-immune-cell secreted cytokines/chemokines are involved in the regulation of metabolic homeostasis as well as the development of metabolic diseases such as diabetes, obesity, and cardiovascular diseases. To further study muscle cell cytokines/chemokines secretion systematically, we collected mouse muscle cell (C2C12) culture medium samples at Day 0, 1, 3, 5 after cell differentiation and measured cytokine/chemokine concentration in these samples using MILLIPLEX® map Mouse Cytokine/Chemokine Panels I (32 analytes), II (12 analytes), and III (6 analytes) multiplex assays using the Luminex® xMAP® technology. Among the 50 cytokines/chemokines measured we found 9 cytokines/chemokines were easily detectable in C2C12 culture medium samples. Six of them, including IL-6, Eotaxin, IP-10, VEGF, Fractalkine, and TARC, showed a gradual concentration increase after cell differentiation. These data demonstrated that MILLIPLEX® map Mouse Cytokine/Chemokine panels are useful tools for cytokine/chemokine secretion profiling and indicate that muscle cells may secrete more myokines than have been previously reported.

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Matsumoto, Ari, Miki Hiroi, Kazumasa Mori, Nobuharu Yamamoto, and Yoshihiro Ohmori. "Differential Anti-Tumor Effects of IFN-Inducible Chemokines CXCL9, CXCL10, and CXCL11 on a Mouse Squamous Cell Carcinoma Cell Line." Medical Sciences 11, no. 2 (April 25, 2023): 31. http://dx.doi.org/10.3390/medsci11020031.

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Chemokines are a group of cytokines involved in the mobilization of leukocytes, which play a role in host defense and a variety of pathological conditions, including cancer. Interferon (IFN)-inducible chemokines C-X-C motif ligand 9 (CXCL), CXCL10, and CXCL11 are anti-tumor chemokines; however, the differential anti-tumor effects of IFN-inducible chemokines are not completely understood. In this study, we investigated the anti-tumor effects of IFN-inducible chemokines by transferring chemokine expression vectors into a mouse squamous cell carcinoma cell line, SCCVII, to generate a cell line stably expressing chemokines and transplanted it into nude mice. The results showed that CXCL9- and CXCL11-expressing cells markedly inhibited tumor growth, whereas CXCL10-expressing cells did not inhibit growth. The NH2-terminal amino acid sequence of mouse CXCL10 contains a cleavage sequence by dipeptidyl peptidase 4 (DPP4), an enzyme that cleaves the peptide chain of chemokines. IHC staining indicated DPP4 expression in the stromal tissue, suggesting CXCL10 inactivation. These results suggest that the anti-tumor effects of IFN-inducible chemokines are affected by the expression of chemokine-cleaving enzymes in tumor tissues.

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Zhang, Peng-Fei, Chuang Wang, Le Zhang, and Qiu Li. "Reversing chemokine/chemokine receptor mismatch to enhance the antitumor efficacy of CAR-T cells." Immunotherapy 14, no. 6 (April 2022): 459–73. http://dx.doi.org/10.2217/imt-2021-0228.

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Currently, the antitumor efficacy of chimeric antigen receptor T cells in solid tumors is modest. Both chemokines and their receptors play a key role in the proliferation of cancer cells, tumor angiogenesis, organ-selective metastasis and migration of immune cells to solid tumors. Unfortunately, frequent chemokine/chemokine receptor ‘mismatch’ between effector cells and the tumor microenvironment results in inefficient T-cell infiltration and antitumor efficacy. Thus, reversing the ‘mismatch’ of chemokines and chemokine receptors appears to be a promising method for promoting T-cell infiltration into the tumor and enhancing their antitumor efficacy. In this review, we discuss functions of the chemokine/chemokine receptor axis in cancer immunity and the current understanding, challenges and prospects for improving the effect of chimeric antigen receptor T cells by reversing the mismatch between chemokines and chemokine receptors.

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Olson, Timothy S., and Klaus Ley. "Chemokines and chemokine receptors in leukocyte trafficking." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, no. 1 (July 1, 2002): R7—R28. http://dx.doi.org/10.1152/ajpregu.00738.2001.

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Chemokines regulate inflammation, leukocyte trafficking, and immune cell differentiation. The role of chemokines in homing of naive T lymphocytes to secondary lymphatic organs is probably the best understood of these processes, and information on chemokines in inflammation, asthma, and neurological diseases is rapidly increasing. Over the past 15 years, understanding of the size and functional complexity of the chemokine family of peptide chemoattractants has grown substantially. In this review, we first present information regarding the structure, expression, and signaling properties of chemokines and their receptors. The second part is a systems physiology-based overview of the roles that chemokines play in tissue-specific homing of lymphocyte subsets and in trafficking of inflammatory cells. This review draws on recent experimental findings as well as current models proposed by experts in the chemokine field.

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van Berkel, Victor, John Barrett, H. Lee Tiffany, Daved H. Fremont, Philip M. Murphy, Grant McFadden, Samuel H. Speck, and Herbert W. Virgin. "Identification of a Gammaherpesvirus Selective Chemokine Binding Protein That Inhibits Chemokine Action." Journal of Virology 74, no. 15 (August 1, 2000): 6741–47. http://dx.doi.org/10.1128/jvi.74.15.6741-6747.2000.

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ABSTRACT Chemokines are involved in recruitment and activation of hematopoietic cells at sites of infection and inflammation. The M3 gene of γHV68, a gamma-2 herpesvirus that infects and establishes a lifelong latent infection and chronic vasculitis in mice, encodes an abundant secreted protein during productive infection. The M3 gene is located in a region of the genome that is transcribed during latency. We report here that the M3 protein is a high-affinity broad-spectrum chemokine scavenger. The M3 protein bound the CC chemokines human regulated upon activation of normal T-cell expressed and secreted (RANTES), murine macrophage inflammatory protein 1α (MIP-1α), and murine monocyte chemoattractant protein 1 (MCP-1), as well as the human CXC chemokine interleukin-8, the murine C chemokine lymphotactin, and the murine CX3C chemokine fractalkine with high affinity (Kd = 1.6 to 18.7 nM). M3 protein chemokine binding was selective, since the protein did not bind seven other CXC chemokines (Kd > 1 μM). Furthermore, the M3 protein abolished calcium signaling in response to murine MIP-1α and murine MCP-1 and not to murine KC or human stromal cell-derived factor 1 (SDF-1), consistent with the binding data. The M3 protein was also capable of blocking the function of human CC and CXC chemokines, indicating the potential for therapeutic applications. Since the M3 protein lacks homology to known chemokines, chemokine receptors, or chemokine binding proteins, these studies suggest a novel herpesvirus mechanism of immune evasion.

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Ji, Guang. "Advances in Research on the Role of Chemokines in Occurrence and Development of Autoimmune Thyroid Disease." Infection International 4, no. 3 (September 1, 2015): 59–63. http://dx.doi.org/10.1515/ii-2017-0108.

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AbstractChemokines can be divided into four categories: α, β, γ, and δ. Chemokine α is related to neutrophil chemotaxis. Chemokine β is correlated with adsorption of monocytes, basophils, and eosinophils. Chemokine γ is mainly a lymphocyte chemokine. Function of chemokine δ remains unclear. Chemokines α and β are primarily related to occurrence and development of autoimmune thyroid disease. This study reviews chemokines and their receptors that are related to Graves’ disease and Hashimoto’s thyroiditis.

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McKenna, Sophie, Sean Patrick Giblin, Rosemarie Anne Bunn, Yingqi Xu, Stephen John Matthews, and James Edward Pease. "A highly efficient method for the production and purification of recombinant human CXCL8." PLOS ONE 16, no. 10 (October 15, 2021): e0258270. http://dx.doi.org/10.1371/journal.pone.0258270.

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Chemokines play diverse and fundamental roles in the immune system and human disease, which has prompted their structural and functional characterisation. Production of recombinant chemokines that are folded and bioactive is vital to their study but is limited by the stringent requirements of a native N-terminus for receptor activation and correct disulphide bonding required to stabilise the chemokine fold. Even when expressed as fusion proteins, overexpression of chemokines in E. coli tends to result in the formation of inclusion bodies, generating the additional steps of solubilisation and refolding. Here we present a novel method for producing soluble chemokines in relatively large amounts via a simple two-step purification procedure with no requirements for refolding. CXCL8 produced by this method has the correct chemokine fold as determined by NMR spectroscopy and in chemotaxis assays was indistinguishable from commercially available chemokines. We believe that this protocol significantly streamlines the generation of recombinant chemokines.

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Segerer, Stephan, and Peter J. Nelson. "Chemokines in Renal Diseases." Scientific World JOURNAL 5 (2005): 835–44. http://dx.doi.org/10.1100/tsw.2005.105.

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The chemokines, members of a large family of chemotactic cytokines, act as directional cues for sorting inflammatory cell subsets to sites of inflammation or lymphoid microenvironments. In addition to their effects on migration, chemokines can also activate effector function in leukocytes and are involved in cell proliferation and angiogenesis. Therefore, it is not surprising that chemokines play important roles in a wide range of human diseases, including genetic immunodeficiencies, infections, autoimmune diseases, and malignant tumors. In this report, we have reviewed recent developments (since mid 2003) in chemokines in renal diseases. In animal models, chemokines are produced at the site of injury, leading to inflammatory cell recruitment. The therapeutic impact of the blockade of CCR1, CCR2, CCR4, CCR5, or the corresponding ligands has been further studied in various renal disease models. Recent studies on the role of the chemokine receptors in human diseases have demonstrated the expression of CXCR1, CXCR3, CCR2, and CCR5 on different subsets of inflammatory cells. The number of CCR5- and CXCR3-positive interstitial infiltrating cells (mainly T cells) correlates with renal function and proteinuria in glomerular diseases. Polymorphisms of chemokines and chemokine receptors are of impact on renal disease courses and allograft survival. Chemokine receptor blockade has approached clinical applications in nonrenal diseases and awaits the application in patients with kidney diseases.

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Luesink, Maaike, Jeroen L. A. Pennings, Willemijn M. Wissink, Peter C. M. Linssen, Petra Muus, Rolph Pfundt, Theo J. M. de Witte, Bert A. van der Reijden, and Joop H. Jansen. "Chemokine induction by all-trans retinoic acid and arsenic trioxide in acute promyelocytic leukemia: triggering the differentiation syndrome." Blood 114, no. 27 (December 24, 2009): 5512–21. http://dx.doi.org/10.1182/blood-2009-02-204834.

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Abstract In acute promyelocytic leukemia (APL), differentiation therapy with all-trans retinoic acid (ATRA) and/or arsenic trioxide can induce a differentiation syndrome (DS) with massive pulmonary infiltration of differentiating leukemic cells. Because chemokines are implicated in migration and extravasation of leukemic cells, chemokines might play a role in DS. ATRA stimulation of the APL cell line NB4 induced expression of multiple CC-chemokines (CCLs) and their receptors (> 19-fold), resulting in increased chemokine levels and chemotaxis. Induction of CCL2 and CCL24 was directly mediated by ligand-activated retinoic acid receptors. In primary leukemia cells derived from APL patients at diagnosis, ATRA induced chemokine production as well. Furthermore, in plasma of an APL patient with DS, we observed chemokine induction, suggesting that chemokines might be important in DS. Dexamethasone, which efficiently reduces pulmonary chemokine production, did not inhibit chemokine induction in APL cells. Finally, chemokine production was also induced by arsenic trioxide as single agent or in combination with ATRA. We propose that differentiation therapy may induce chemokine production in the lung and in APL cells, which both trigger migration of leukemic cells. Because dexamethasone does not efficiently reduce leukemic chemokine production, pulmonary infiltration of leukemic cells may induce an uncontrollable hyperinflammatory reaction in the lung.

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Red-Horse, Kristy, Penelope M. Drake, and Susan J. Fisher. "Human pregnancy: the role of chemokine networks at the fetal–maternal interface." Expert Reviews in Molecular Medicine 6, no. 11 (May 7, 2004): 1–14. http://dx.doi.org/10.1017/s1462399404007720.

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Chemokines are multifunctional molecules initially described as having a role in leukocyte trafficking and later found to participate in developmental processes such as differentiation and directed migration. Similar events occur in pregnancy during development of the fetal–maternal interface, where there is extensive leukocyte trafficking and tissue morphogenesis, and this is accompanied by abundant chemokine expression. The relationship between chemokines, leukocytes and placental development is beginning to be delineated. During pregnancy a specialised population of maternal leukocytes infiltrates the implantation site. These leukocytes are thought to sustain the delicate balance between protecting the developing embryo/fetus and tolerating its hemiallogeneic tissues. A network of chemokine expression by both fetal and maternal components in the pregnant uterus functions in establishing this leukocyte population. Intriguingly, experiments investigating immune cell recruitment revealed the additional possibility that chemokines influence aspects of placental development. Specifically, cytotrophoblasts, the effector cells of the placenta, express chemokine receptors that can bind ligands found at key locations, implicating chemokines as regulators of cytotrophoblast differentiation and migration. Thus, as in other systems, at the fetal–maternal interface chemokines might regulate multiple functions.

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McKimmie, C. S., and G. J. Graham. "Leucocyte expression of the chemokine scavenger D6." Biochemical Society Transactions 34, no. 6 (October 25, 2006): 1002–4. http://dx.doi.org/10.1042/bst0341002.

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Selective sequestration of inflammatory chemokines is critical for the successful resolution of inflammatory responses in vivo. D6 is an atypical chemokine receptor that scavenges inflammatory chemokines and is pivotal in resolving models of chemokine-driven cutaneous inflammation. We provide evidence that expression of D6 is not limited to the lymphatic endothelium at sites of inflammation as previously believed. Instead we postulate that D6 expression in leucocytes may have a significant impact upon chemokine bioavailability during the resolution phase of inflammation. D6 expressed on the lymphatic endothelia may instead have complementary roles in preventing inappropriate leucocyte migration to the lymph node by keeping the endothelium free from inflammatory chemokines.

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Kaffashi, Kimia, Didier Dréau, and Irina V. Nesmelova. "Heterodimers Are an Integral Component of Chemokine Signaling Repertoire." International Journal of Molecular Sciences 24, no. 14 (July 19, 2023): 11639. http://dx.doi.org/10.3390/ijms241411639.

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Chemokines are a family of signaling proteins that play a crucial role in cell–cell communication, cell migration, and cell trafficking, particularly leukocytes, under both normal and pathological conditions. The oligomerization state of chemokines influences their biological activity. The heterooligomerization occurs when multiple chemokines spatially and temporally co-localize, and it can significantly affect cellular responses. Recently, obligate heterodimers have emerged as tools to investigate the activities and molecular mechanisms of chemokine heterodimers, providing valuable insights into their functional roles. This review focuses on the latest progress in understanding the roles of chemokine heterodimers and their contribution to the functioning of the chemokine network.

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Huang, Ziwei, Santosh Kumar, Won-Tak Choi, Navid Madani, Chang-Zhi Dong, Dongxiang Liu, Jun Wang, Jing An, and Joseph G. Sodroski. "A New Class of Chemokine Analogs as Useful Research Tools to Study Chemokine Receptor Function and Promising Therapeutic Agents." Blood 104, no. 11 (November 16, 2004): 3839. http://dx.doi.org/10.1182/blood.v104.11.3839.3839.

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Abstract Chemokine receptors play important roles in many physiological processes and are implicated in a wide range of human diseases including acute respiratory distress syndrome, allergic asthma, psoriasis, arthritis, multiple sclerosis, cancer, atherosclerosis and most notably AIDS. To enable the applications of chemokine ligands as probes of receptor biology and pharmacology, and inhibitors of diseases mediated by chemokine receptors, a major problem with the lack of receptor selectivity of these natural chemokines must be overcome. In this study, we have developed a chemical approach combining total protein synthesis and modular modifications to generate a new family of unnatural chemokines termed SMM-chemokines (which refer to synthetically and modularly modified chemokines) with designed receptor selectivity and affinity. A proof of the concept has been provided by applying this strategy to transform a very nonselective chemokine vMIP-II into new analogs with enhanced selectivity and potency for CXCR4 or CCR5, two principal coreceptors for HIV-1 entry. Such novel molecules have been shown subsequently to be valuable probes in gaining insights into receptor binding and signaling mechanisms, and as potent inhibitors to prevent HIV-1 entry and infection. These results strongly support the design concept of these SMM-chemokines and suggest that general applicability of this approach for studying and controlling other chemokine receptors and the diseases they mediate might be anticipated.

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Szekanecz, Zoltan. "Chemokines and chemokine receptors in arthritis." Frontiers in Bioscience S2, no. 1 (2010): 153–67. http://dx.doi.org/10.2741/s53.

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Bonecchi, Raffaella. "Chemokines and chemokine receptors: an overview." Frontiers in Bioscience Volume, no. 14 (2009): 540. http://dx.doi.org/10.2741/3261.

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Egido, Jesús. "Chemokines, chemokine receptors and renal disease." Kidney International 56, no. 1 (July 1999): 347–48. http://dx.doi.org/10.1046/j.1523-1755.1999.00551.x.

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Nelson, Peter J., and Alan M. Krensky. "Chemokines, Chemokine Receptors, and Allograft Rejection." Immunity 14, no. 4 (April 2001): 377–86. http://dx.doi.org/10.1016/s1074-7613(01)00118-2.

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Yamamoto, Toshiyuki. "Chemokines and Chemokine Receptors in Scleroderma." International Archives of Allergy and Immunology 140, no. 4 (2006): 345–56. http://dx.doi.org/10.1159/000094242.

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Kakinuma, T. "Chemokines, chemokine receptors, and cancer metastasis." Journal of Leukocyte Biology 79, no. 4 (January 13, 2006): 639–51. http://dx.doi.org/10.1189/jlb.1105633.

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Karpus, William J., and Brian T. Fife. "Keystone Symposia: chemokines and chemokine receptors." Expert Opinion on Biological Therapy 1, no. 3 (May 2001): 549–53. http://dx.doi.org/10.1517/14712598.1.3.549.

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Frangogiannis, Nikolaos. "Chemokines in ischemia and reperfusion." Thrombosis and Haemostasis 97, no. 05 (2007): 738–47. http://dx.doi.org/10.1160/th07-01-0022.

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SummaryChemokine signaling plays an important role in the postischemic inflammatory response. Overlapping pathways involving reactive oxygen intermediates,Toll-like receptor (TLR) activation, the complement cascade and the nuclear factor (NF)- κ B system induce both CXC and CC chemokines in ischemic tissues. Reperfusion accentuates chemokine expression promoting an intense inflammatory reaction. ELR-containing CXC chemokines regulate neutrophil infiltration in the ischemic area, whereas CXCR3 ligands may mediate recruitment of Th1 cells. CC chemokines, on the other hand, induce mononuclear cell infiltration and macrophage activation.Evidence suggests that chemokine signaling mediates actions beyond leukocyte chemotaxis and activation, regulating angiogenesis and fibrous tissue deposition. Effective repair of ischemic tissue is dependent on a wellorchestrated cellular response and on timely induction and suppression of chemokines in a locally restricted manner. This manuscript reviews the evidence suggesting a role for chemokine- mediated effects in ischemia/reperfusion and discusses the potential significance of these interactions in injury and repair of ischemic tissues.

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Taub, D. D., T. J. Sayers, C. R. Carter, and J. R. Ortaldo. "Alpha and beta chemokines induce NK cell migration and enhance NK-mediated cytolysis." Journal of Immunology 155, no. 8 (October 15, 1995): 3877–88. http://dx.doi.org/10.4049/jimmunol.155.8.3877.

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Abstract Chemokines have been shown to play an important role in both the adhesion and migration of numerous leukocytic cell types, including granulocytes, monocytes, mast cells, and T lymphocytes. However, the biologic effects of chemokines on NK cells remain to be defined. Chemotaxis studies using purified human NK cells and a panel of human recombinant chemokines revealed that macrophage inflammatory protein (MIP)-1 alpha and IFN-inducible protein-10 (IP-10) are potent NK cell chemoattractants in vitro. Modest but significant chemotactic (not chemokinetic) responses were also observed in response to RANTES, MCP-1, MCP-2, MCP-3, and MIP-1 beta. Chemokine receptor expression on human NK cells was determined through displacement and Scatchard analyses, using a panel of radiolabeled chemokines, and revealed the presence of both distinct and shared chemokine receptors with affinities similar to those previously described for other cell types. Functional studies have also revealed that the beta chemokines and IP-10 are capable of augmenting NK- but not LAK- or ADCC-specific cytolytic responses in both a dose- and donor-dependent fashion. Neutralization analysis using Abs specific for various adhesion molecules revealed that NK:tumor cell conjugate formation is required for chemokine-induced NK killing. In addition, NK cells incubated in the presence of beta chemokines and IP-10 for 4 h induced the release of granule-derived serine esterases, suggesting a possible mechanism for chemokine-mediated NK killing. These results suggest that chemokines not only play an important role in the recruitment of NK cells, but also may be important mediators of NK cell degranulation augmenting local tumor cell destruction.

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Groblewska, Magdalena, Ala Litman-Zawadzka, and Barbara Mroczko. "The Role of Selected Chemokines and Their Receptors in the Development of Gliomas." International Journal of Molecular Sciences 21, no. 10 (May 24, 2020): 3704. http://dx.doi.org/10.3390/ijms21103704.

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Among heterogeneous primary tumors of the central nervous system (CNS), gliomas are the most frequent type, with glioblastoma multiforme (GBM) characterized with the worst prognosis. In their development, certain chemokine/receptor axes play important roles and promote proliferation, survival, metastasis, and neoangiogenesis. However, little is known about the significance of atypical receptors for chemokines (ACKRs) in these tumors. The objective of the study was to present the role of chemokines and their conventional and atypical receptors in CNS tumors. Therefore, we performed a thorough search for literature concerning our investigation via the PubMed database. We describe biological functions of chemokines/chemokine receptors from various groups and their significance in carcinogenesis, cancer-related inflammation, neo-angiogenesis, tumor growth, and metastasis. Furthermore, we discuss the role of chemokines in glioma development, with particular regard to their function in the transition from low-grade to high-grade tumors and angiogenic switch. We also depict various chemokine/receptor axes, such as CXCL8-CXCR1/2, CXCL12-CXCR4, CXCL16-CXCR6, CX3CL1-CX3CR1, CCL2-CCR2, and CCL5-CCR5 of special importance in gliomas, as well as atypical chemokine receptors ACKR1-4, CCRL2, and PITPMN3. Additionally, the diagnostic significance and usefulness of the measurement of some chemokines and their receptors in the blood and cerebrospinal fluid (CSF) of glioma patients is also presented.

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Journal articles on the topic 'Chemokines'

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