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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.Cite
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The chemokine system has evolved primarily to control the trafficking of leukocytes during immune or inflammatory responses. However, through their expression of chemokine ligands and receptors, cancers have commandeered various aspects of this host defence system in order to enhance their growth. Although engineered over-expression of some tumour-derived chemokines can stimulate host antitumour respones, this is unlikely to be the reason that tumour cells express them. Rather, a growing body of clinical and laboratory evidence indicates that cancer cells may secrete chemokines in order to attract host cells that supply the tumours with growth and angiogenic factors. In addition, chemokine receptor expression by tumour cells may permit them to use the host's pre-existing leukocyte trafficking system to invade target tissues during metastatic spread. Together, these observations suggest that therapies directed against chemokine ligands or receptors may be beneficial in cancer.
CCR10
Chemokine receptor CCR5
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CXC chemokine receptors
Chemokine receptor CCR5
Medical microbiology
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Abstract Directed migration and arrest of leukocytes during homeostasis, inflammation, and tumor development is mediated by the chemokine system, which governs leukocyte migration and activities. Although we understand well the effects of different chemokines one by one, much less was known about the potential consequences of the concomitant expression of multiple chemokines or of their interaction with inflammatory molecules on leukocyte migration and functions. In the past 10 yr, several studies revealed the existence of additional features of chemokines: they can antagonize chemokine receptors or synergize with other chemokines, also by forming heterocomplexes. Moreover, recent data show that not only chemokines but also the alarmin high-mobility group box 1 can for a complex with CXCL12, enhancing its potency on CXCR4. The molecular mechanism underlying the effect of the heterocomplex has been partially elucidated, whereas its structure is a matter of current investigations. The present review discusses the current knowledge and relevance of the functions of heterocomplexes formed between chemokines or between the chemokine CXCL12 and the alarmin high-mobility group box 1. These studies highlight the importance of taking into account, when approaching innovative therapies targeting the chemokine system, also the fact that some chemokines and molecules released in inflammation, can considerably affect the activity of chemokine receptor agonists.
Modulation (music)
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Cell surface receptor
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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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Radiotherapy plays an important role in the treatment of malignant head and neck tumors. Chemokines are chemotactic cytokines, which can induce tumor proliferation as well as metastasis, although the influence of chemokines and their signaling pathways via chemokine receptors is not fully understood. Moreover, the radiation-induced expression of chemokines and chemokine receptors is poorly studied. Therefore, the purpose of this work was to analyze the expression of the chemokines of the CC-and CXC-class and their receptors in untreated and in irradiated squamous cell carcinoma of the head and neck (SCCHN). The expression of chemokines and chemokine receptors in 15 head and neck carcinoma cell lines and two normal tissue cell lines was analyzed. The spontaneous expression and the expression 6 hours after irradiation with 2 Gy was determined. To validate the results, certain chemokines and chemokine receptors were re-analyzed in selected cell lines. In this second independent analysis the expression was detected for 48 hours after irradiation. Gene expression of chemokines and their receptors was detected by real-time PCR. In addition, the protein expression of two chemokines was analyzed by ELISA. The results of the first analysis showed, that the chemokine receptors were less widely expressed in the investigated cell lines than the chemokines. Irradiation with 2 Gy caused an altered expression of the chemokines and chemokine receptors in all investigated cell lines. Radiation caused up- and downregulation in the expression of the chemokines, whereas the expression of the investigated receptors was predominantly downregulated after irradiation. The results of the chemokine expression were validated in the second, independent analysis. Radiation caused again up- and downregulation in the expression of the chemokines, but also showed that the expression of the chemokines and its receptors varies over the entire period of 48 hours after irradiation. The protein expression of the chemokines CXCL1 and CXCL12 corresponded well with the mRNA expression. In summary, irradiation of squamous cell carcinoma of the head and neck (SCCHN) and normal tissue cells caused a radiation-induced change of gene expression of the chemokine and its receptors. The results of this analysis show the complexity of the topic, so further studies will be needed to fully understand the influence of chemokines and chemokine receptors and their effect under a treatment of squamous cell carcinoma of the head and neck.
CCR10
CCL7
CXC chemokine receptors
CCR3
CCL13
CCR1
CCL21
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Monocyte
CCR2
CCR1
CCL13
CC chemokine receptors
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Abstract The discovery of HIV-1-suppressive chemokines and the subsequent discovery of their cognate receptors as coreceptors for HIV-1 entry herald a paradigmatic shift in the study of HIV-1 pathogenesis. The presence of polymorphisms in chemokine receptor and chemokine genes associated with altered progression and susceptibility to the HIV-1 disease further underscores the potential importance that chemokines and their cognate receptors play in HIV-1 pathogenesis. It has become increasingly apparent that the immune system maintains a delicate balance between the positive and negative regulators that govern the chemokine and cytokine networks. Here we review the most recent developments in chemokine biology and relate how research into their structure, regulation, and the mechanism of their actions can shed light on the immunopathogenesis of HIV-1 disease. J. Leukoc. Biol. 65: 552–565; 1999.
Pathogenesis
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