Relevant bibliographies by topics / Chemokine

Academic literature on the topic 'Chemokine'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 July 2024

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Journal articles on the topic "Chemokine"

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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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Hansell, C. A. H., C. V. Simpson, and R. J. B. Nibbs. "Chemokine sequestration by atypical chemokine receptors." Biochemical Society Transactions 34, no. 6 (October 25, 2006): 1009–13. http://dx.doi.org/10.1042/bst0341009.

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Leucocyte migration is essential for robust immune and inflammatory responses, and plays a critical role in many human diseases. Chemokines, a family of small secreted protein chemoattractants, are of fundamental importance in this process, directing leucocyte trafficking by signalling through heptahelical G-protein-coupled receptors expressed by the migrating cells. However, several mammalian chemokine receptors, including D6 and CCX-CKR (ChemoCentryx chemokine receptor), do not fit existing models of chemokine receptor function, and do not even appear to signal in response to chemokine binding. Instead, these ‘atypical’ chemokine receptors are biochemically specialized for chemokine sequestration, acting to regulate chemokine bioavailability and thereby influence responses through signalling-competent chemokine receptors. This is of critical importance in vivo, as mice lacking D6 show exaggerated cutaneous inflammatory responses and an increased susceptibility to the development of skin cancer. CCX-CKR, on the other hand, is predicted to modulate homoeostatic lymphocyte and dendritic cell trafficking, key migratory events in acquired immune responses that are directed by CCX-CKR-binding chemokines. Thus studies on ‘atypical’ chemokine receptors are revealing functional and biochemical diversity within the chemokine receptor family and providing insights into novel mechanisms of chemokine regulation.
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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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Romero, Joan Miguel, Emma Titmuss, Yifan Wang, James Vafiadis, Alain Pacis, Gun Ho Jang, Amy Zhang, et al. "Assessment of a 4-chemokine signature in prediction of T-cell inflammation and response to immune checkpoint inhibition across tumor types." Journal of Clinical Oncology 40, no. 16_suppl (June 1, 2022): 2558. http://dx.doi.org/10.1200/jco.2022.40.16_suppl.2558.

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2558 Background: Immune checkpoint inhibitors (ICI) are highly effective in select cancers. Novel predictors of T cell-inflammation may identify a broader subset of tumors with ICI responsiveness. Our group has identified four chemokines (CCL4, CCL5, CXCL9, CXLC10) able to predict a T cell-inflamed phenotype in primary and metastatic pancreatic tumors. Here, we test whether this 4-chemokine signature can predict T cell-inflammation across additional tumor types and response to ICI. Methods: Using matched genomic and transcriptomic data from 6,455 patients spanning 25 tumor types from The Cancer Genome Atlas, we searched for associations between the 4-chemokine signature and metrics of antitumor immunity. Further, we tested the association of this signature with markers of DNA damage repair deficiency. We also investigated the ability of this signature to predict response to immunotherapy using real-world data from a pan-cancer cohort of 82 patients in the Personalized OncoGenomics Program who had received ICI. Results: The majority of tumor types displayed sub-populations with high expression of the 4-chemokines (4-chemokinehi) and transcriptional hallmarks of the cancer-immunity cycle. Testicular germ cell tumors, cervical squamous cell carcinomas, and head and neck squamous cell carcinomas were the strongest expressors of the signature. Immunomodulatory genes, including PD-L1, PD-1, TIM3, LAG3, TIGIT, CTLA-4, and FASLG, were significantly overexpressed (p<0.05) in the 4-chemokinehi cohorts. Genesets of processes involved in the cancer-immunity cycle, including MHC I expression and cytolytic activity, were upregulated in the 4-chemokinehi cohorts (p<0.05). While a global relationship between tumor mutation burden (TMB) and 4-chemokine expression across tumor histological type was seen (rho=0.42, p=0.02), high TMB was associated with only a subset of 4-chemokinehi tumors. Among patients treated with ICIs, those with 4-chemokinehi tumors had a longer median time to progression (104 versus 71 days, p=0.013) and overall survival (391 versus 195 days, p=0.016). The 4-chemokine signature outperformed TMB for overall survival prediction. Conclusions: Sub-populations of T cell-inflamed patients exist across tumor types and may therefore respond favourably to ICI. The 4-chemokine signature has the potential to select a wider spectrum of patients that may benefit from ICIs. [Table: see text]
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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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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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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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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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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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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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Dissertations / Theses on the topic "Chemokine"

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Hua, Renyi. "The role of chemokines/chemokine receptors in labour." Thesis, Imperial College London, 2012. http://hdl.handle.net/10044/1/9847.

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Human labour is shown to be an inflammatory process, which involves a marked leukocyte infiltrate into myometrium during labour. My study focused on the role of chemokines, key mediators of leukocyte trafficking, in labour. Previous gene array data obtained from human labouring myometrium showed that the mRNA expression of the following chemokines was increased in term labouring myometrium, CCL2, CCL20, CXCL1, CXCL5, CXCL8. I decided to focus on myometrial expression of these chemokines and also to include CCL5, another important chemokine. My data confirmed that the expression of human myometrial chemokines was increased in labour and that their expression was up regulated by cytokines and mechanical stretch via NFKB and MAPK, but decreased by prostaglandins and oxytocin via PLC. I also studied the expression of myometrial chemokine receptors, which may mediate some of the effects of chemokines on myometrial function and/or act as decoys, minimising the effects of locally produced chemokines. I found that the expression of the chemokine receptors decreased with the onset of labour, mainly through the action of prostaglandins and oxytocin. I then used the established model of LPS-­‐induced preterm labour (PTL) in the mouse and found that chemokines and cytokines both increased in the myometrium and placenta. CCL2 is consistently increased with human labour and has been shown to be important in rodent parturition too. I therefore studied the impact of LPS in the CCR2 (the main receptor for CCL2) knockout mouse. There was less inflammation in both the myometrium and placenta and a better pup survival rate in the CCR2-/- mouse. However, the PTL was not delayed, suggesting that CCR2 is not essential for the induction of PTL labour by LPS in the mouse. I then turned my attention to CCL20, which acts only via CCR6. It is known to drive dendritic cell recruitment and I found that its expression was increased with labour, while that of its receptor was reduced. Functionally, I found that CCL20 up-regulated the myometrial expression of chemokines. Next I used the LPS-induced preterm labour model in the mouse and found that CCR6 knockout delayed LPS-induced preterm delivery and improved pup survival. These findings were associated with much lower inflammation in myometrium and plasma. These data suggest that CCR6 could be a therapeutic target in the management of PTL. Chemokines play an important role both in the induction of term labour and in infection induced PTL. Chemokine inhibitors may delay the onset of PTL and improve the fetal outcome.
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Wong, Jeffrey K. W. "Chemokines and chemokine receptors in islet xenograft rejection." Thesis, The University of Sydney, 2006. https://hdl.handle.net/2123/28055.

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This project investigates the role of chemokine and chemokine receptors in a model of CD4 T cell dependent cellular xenograft rejection, specifically the transplantation of fetal pig pancreas tissue to the renal subcapsular space of mice. Chemokines and chemokine receptor gene expression was assessed by cDNA arrays, and confirmed by multi-probe ribonuclease protection assay. Immunostaining for a selected chemokine, RANTES was performed to demonstrate upregulation at the protein level. These methods were applied to several different models to dissect the role Chemokines and their receptors in this process. Comparisons were made with: an allografi model, a model where indefinite xenograft survival could be achieved by short term costimulatory blockade with CTLA4-Fc and MR1, and an immunodeficient mouse recipient (RAG—1 KO, lacks B and T cells) that was reconstituted with either unfractionated leucocytes or purified CD4 T cells. The main findings were: 1. Allograft rejection and cellular xenografi rejection are THl type CD4 T cell dependent processes as shown by the common T cell chemokine genes (Ltn, IP-lO, and Mig) expressed in both models; however macrophages are the main effector cell in cellular xenografi rejection as evidenced by the selective upregulation of MCP-l and its receptor CCR2, as well as other macrophage markers 2. Of the Chemokines / receptors upregulated in this model of cellular xenograft rejection (Ltn, IP-lO, MCP-l, RANTES, MIP-lB, eotaxin) only MCP-l and IP-lO are CD4 T cell dependent, while Ltn expression is dependent upon a non-CD4 T cell leucocyte subset. 3. CTLA4-Fc and MR1 therapy resulted in indefinite fetal porcine islet survival and function in diabetic immune competent wild type C57BL/6 mice. This treatment suppresses the early upregulation of chemokines and chemokine receptors seen in untreated animals, and this corresponds with a significant reduction CD4 T cell and macrophage grafi infiltration at these time points, consistent with a role for select chemokine / receptors in the mechanism by which this therapy leads to indefinite graft survival. 4. In addition we studied the functioning of fetal porcine islet tissue in diabetic mice and found they developed and controlled glucose metabolism in a piglike manner, and different to normal mice, and thus conclude the development and function of fetal tissue in cross species transplantation is dependent upon the origins of the progenitor cells and not the xenogeneic environment i.e. nature not nurture (in this case anyway). We conclude that select chemokines and their receptors are important factors in the recruitment of effector cells mediating graft rejection in this model of cellular xenograft rejection and these chemokine pathways and networks may represent potential future therapeutic targets.
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Mowafi, Frida. "Chemokines and chemokine receptors during viral infections in man /." Stockholm : Karolinska institutet, 2007. http://diss.kib.ki.se/2007/978-91-7357-420-4/.

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Davis, Christopher Nathan. "Mammalian and viral chemokines provide insight into the mechanism of chemokine receptor activation." [Gainesville, Fla.] : University of Florida, 2004. http://purl.fcla.edu/fcla/etd/UFE0006481.

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Wang, Jixin. "Bioinformatic analysis of chicken chemokines, chemokine receptors, and Toll-like receptor 21." Texas A&M University, 2006. http://hdl.handle.net/1969.1/4212.

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Chemokines triggered by Toll-like receptors (TLRs) are small chemoattractant proteins, which mainly regulate leukocyte trafficking in inflammatory reactions via interaction with G protein-coupled receptors. Forty-two chemokines and 19 cognate receptors have been found in the human genome. Prior to this study, only 11 chicken chemokines and 7 receptors had been reported. The objectives of this study were to identify systematically chicken chemokines and their cognate receptor genes in the chicken genome and to annotate these genes and ligand-receptor binding by a comparative genomics approach. Twenty-three chemokine and 14 chemokine receptor genes were identified in the chicken genome. The number of coding exons in these genes and the syntenies are highly conserved between human, mouse, and chicken although the amino acid sequence homologies are generally low between mammalian and chicken chemokines. Chicken genes were named with the systematic nomenclature used in humans and mice based on phylogeny, synteny, and sequence homology. The independent nomenclature of chicken chemokines and chemokine receptors suggests that the chicken may have ligand-receptor pairings similar to mammals. The TLR family represents evolutionarily conserved components of the patternrecognizing receptors (PRRs) of the innate immune system that recognize specific pathogen-associated molecular patterns (PAMPs) through their ectodomains (ECDs). TLR's ECDs contain 19 to 25 tandem copies of leucine-rich repeat (LRR) motifs. TLRs play important roles in the activation of pro-inflammatory cytokines, chemokines and modulation of antigen-specific adaptive immune responses. To date, nine TLRs have been reported in chicken, along with a non-functional TLR8. Two non-mammalian TLRs, TLR21 and TLR22, have been identified in pufferfish and zebrafish. The objectives of this study were to determine if there is the existence of chicken genes homologous to fish-specific TLRs, and if possible ligands of these receptors exist. After searching the chicken genome sequence and EST database, a novel chicken TLR homologous to fish TLR21 was identified. Phylogenetic analysis indicated that the identified chicken TLR is the orthologue of TLR21 in fish. Bioinformatic analysis of potential PAMP binding sites within LRR insertions showed that CpG DNA is the putative ligand of this receptor.
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Teleshova, Natalia. "Studies on co-stimulatory molecules, chemokines and chemokine receptors in neuroimmunological diseases /." Stockholm, 2001. http://diss.kib.ki.se/2001/91-628-4781-3/.

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Maru, Seema V. "The role of chemokines and chemokine receptors in astrocytes and astrocytoma biology." Thesis, Open University, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.427496.

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Brozyna, Sheree. "The role of chemokines and chemokine receptors in chronic obstructive pulmonary disease (COPD) /." Title page and abstract only, 2005. http://web4.library.adelaide.edu.au/theses/09SB/09sbb8859.pdf.

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Schweneker, Marc. "Identification and characterization of two novel proteins interacting with the chemokine- and HIV-1 co-receptor CCR5." [S.l.] : [s.n.], 2004. http://www.diss.fu-berlin.de/2004/22/index.html.

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Fouillet, Antoine. "Cytokines regulation of chemokine and chemokine receptor in relation to multiple sclerosis." Thesis, Sheffield Hallam University, 2008. http://shura.shu.ac.uk/19675/.

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Expression of chemokines CXCL10 and CCL2 is elevated within inflammatory lesions in the central nervous system (CNS) of multiple sclerosis (MS) patients, particularly in astrocytes. These chemokines play a critical role in the recruitment of inflammatory cells into the CNS during inflammation. However, the cerebrospinal fluid of MS patients also shows high levels of CXCL10 at the time of relapse but by contrast CCL2 is decreased. In the present study, the mechanisms controlling the synthesis and release of these two chemokines in MS were assessed in vitro using primary human brain astrocytes isolated from MS and non-MS individuals. Pro-inflammatory cytokines (interleukin-1beta , tumour necrosis factor and interferon-gamma) increased the expression of both CCL2 and CXCL10 by astrocytes at the mRNA and protein level, as determined by real time PCR and enzyme linked immunosorbent assays (ELISA), respectively. CCL2 binding to astrocytes was then determined to evaluate any autocrine action on astrocytes in a single astrocyte preparation. CCL2 bound constitutively and following cytokine treatment. CCL2-binding was not the result of the interaction with its receptor since astrocytes did not express CCR2 on this astrocyte culture. CCR2-independent binding of CCL2 was confirmed by the absence of intracellular signalling, evidenced by the lack of calcium influx as well as of Erk and Akt phosphorylation, in CCL2-treated astrocytes. Even though astrocytes expressed CXCR3, similar negative results on calcium influx and downstream signalling pathways were observed for CXCL10. D6 chemokine decoy receptor expression was then assessed in vitro and in situ to further investigate the mechanism(s) of chemokine binding to astrocytes. Cultured astrocytes constitutively expressed the D6 decoy receptor at the mRNA and protein level, but levels were unchanged following cytokine treatment. D6 was expressed in situ in MS normal appearing white matter and in control brain tissue, at both the mRNA and protein level. D6 expression was detected on neurons and microglia but not astrocytes using imunohistochemical methods. Incubation of frozen brain sections with biotinylated CCL2 resulted in partial co-localisation with D6 staining. Altogether, these results suggest a role for astrocytes in regulating inflammation through synthesis and secretion of CCL2 and CXCL10. Subsequently, CCL2 binding to astrocytes, either by binding to D6 decoy receptor or by alternative mechanisms, may establish a chemokine gradient in the CNS, and direct the migration of leukocytes.
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Books on the topic "Chemokine"

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1956-, Moser Bernhard, Letts Gordon L, and Neote Kuldeep, eds. Chemokine biology: Basic research and clinical application. Basel: Birkhäuser, 2005.

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I, Proudfoot Amanda E., Wells Timothy N. C, and Power Christine, eds. Chemokine protocols. Totowa, N.J: Humana Press, 2000.

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Proudfoot, Amanda E. I., Timothy N. C. Wells, and Christine Power. Chemokine Protocols. New Jersey: Humana Press, 2000. http://dx.doi.org/10.1385/1592590586.

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Richard, Horuk, ed. Chemokine receptors. San Diego: Academic Press, 1997.

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Harrison, Jeffrey K., and Nicholas W. Lukacs, eds. The Chemokine Receptors. Totowa, NJ: Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-020-1.

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Lucas, Alexandra R., ed. Chemokine-Glycosaminoglycan Interactions. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-2835-5.

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Vaddi, Kris. The chemokine factsbook. San Diego: Academic Press, 1997.

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K, Harrison Jeffrey, and Lukacs Nicholas W, eds. The chemokine receptors. Totowa, N.J: Humana, 2007.

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Vaddi, Krishna. The chemokine factsbook. San Diego: Academic Press, 1997.

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1950-, O'Brien Thomas, ed. Chemokine receptors and AIDS. New York: Marcel Dekker, 2002.

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Book chapters on the topic "Chemokine"

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Szekanecz, Zoltán, and Alisa E. Koch. "Chemokines and chemokine receptors." In New Therapeutic Targets in Rheumatoid Arthritis, 129–53. Basel: Birkhäuser Basel, 2009. http://dx.doi.org/10.1007/978-3-7643-8238-4_8.

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Mantovani, A., P. Allavena, C. Garlanda, S. Ramponi, C. Paganini, A. Vecchi, and S. Sozzani. "Chemokines and Chemokine Receptors." In From Basic Immunology to Immune-Mediated Demyelination, 58–67. Milano: Springer Milan, 1999. http://dx.doi.org/10.1007/978-88-470-2143-3_7.

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Luster, Andrew D., and James MacLean. "Chemokines and Chemokine Receptors." In Physiology of Inflammation, 90–110. New York, NY: Springer New York, 2001. http://dx.doi.org/10.1007/978-1-4614-7512-5_6.

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Gressner, A. M., and O. A. Gressner. "Chemokine." In Springer Reference Medizin, 561. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_713.

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Gressner, A. M., and O. A. Gressner. "Chemokine." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_713-1.

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Baggiolini, M. "Introduction to Chemokines and Chemokine Antagonists." In Chemokine Roles in Immunoregulation and Disease, 1–9. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-662-05403-1_1.

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Islam, Sabina A., Benjamin D. Medoff, and Andrew D. Luster. "Chemokine and Chemokine Receptor Analysis." In Manual of Molecular and Clinical Laboratory Immunology, 343–56. Washington, DC, USA: ASM Press, 2016. http://dx.doi.org/10.1128/9781555818722.ch37.

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Akekawatchai, Chareeporn, Marina Kochetkova, Jane Holland, and Shaun R. McColl. "Chemokines and Chemokine Receptors in Cancer Progression." In Chemokine Receptors in Cancer, 1–30. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-267-4_1.

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Parsadaniantz, Stéphane Mélik, Ghazal Banisadr, Philippe Sarret, and William Rostène. "Chemokines and Chemokine Receptors in the Brain." In Chemokine Receptors and NeuroAIDS, 173–89. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0793-6_8.

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Schraufstätter, Ingrid U., Hiroshi Takamori, and Robert C. Hoch. "Chemokine receptors." In Chemokines and Skin, 23–35. Basel: Birkhäuser Basel, 1998. http://dx.doi.org/10.1007/978-3-0348-8843-1_2.

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Conference papers on the topic "Chemokine"

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"Impact of Heparan Sulphate Binding Domain of Chemokine CCL21 to Migration of Breast Cancer Cells." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2020. http://dx.doi.org/10.29117/quarfe.2020.0132.

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Lymph node metastasis constitutes a key event in breast cancer progression. Chemokines are small proteins, which can promote metastatic spread by inducing cancer cell migration and invasion. Chemokine function is dependant upon their binding to both cell surface heparan sulphate (HS) molecules and to their specific receptor. Our group has demonstrated a significant increase in chemokine receptor CCR7 expression in cancerous breast epithelia compared to healthy controls. This study is designed to test the hypothesis that a non-HS binding forms of chemokine CCL21 can disrupt the normal response to CCL21, therefore reducing the metastasis of CCR7-expressing cancer cells. Truncated CCL21 chemokine (Δ98- 134 c-terminal basic extension), was synthesised to investigate a possible linkage between chemokine binding capacity and cell activation. Wild type (WT) and mutant-CCL21 were tested for their ability to stimulate a dose-dependent increase in intracellular-free calcium in peripheral blood mononuclear cell (PBMC) and breast cancer epithelial cells MDA-MB-231. Mutant-CCL21 at concentrations 5 and 10nM showed potential to mobilise Ca2+ at levels similar to that produced by WT-CCl21. A series of experiments was performed to determine how deletion of the HS-binding site altered the ability of CCL21 to stimulate chemotaxis within a concentration gradient generated by free solute diffusion. PBMC stimulated to migrate by wild-type CCL21 was not significantly different from that stimulated by mutant (P> 0.05). Similar results were observed in assays using MDA-MB-231 cells. A further series of experiments was performed to compare the potential of WT and mutant-CCL21 to stimulate the migration of cells across endothelium. In contrast to results for trans-filter migration, it was found that the non HSbinding mutant stimulated no increased in transendothelial cell migration above the background at each of the tested concentrations, 10, 30 and 50 nM respectively (P>0.05). However, WT-CCL21 stimulated significant increased PBMC migration at each of the tested concentration (all P <0.001). Furthermore, the effect of heparin on chemotactic properties of WT and mutant- CCL21 was examined. Interestingly, heparin (250 µg/ml) completely inhibit the chemotaxis mediated by WT-CCL21 (5nM) (P < 0.001), whereas it did not inhibit the chemotaxis at concentrations 100, 250 & 500 µg/ml in response to mutant CCL21 (5nM) (P > 0.05). Similar assay will be performed using MDA-MB-231 cells. Work is ongoing to characterise the biophysical properties of mutant-CCL21 and determine its potential role for a therapeutic blockade of the migration of breast cancer cells in-vivo. Our primarily data showed that mutant CCL21 in xenograft brain tumor models showed substantial inhibition of tumour growth. Our results indicate that truncated CCL21 chemokine might be a potential preventive biofactor for human breast cancer metastasis by targeting chemokine receptor genes.
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Petrek, M., E. Kriegova, R. Fillerova, A. Arakelyan, F. Mrazek, B. Hutyrova, V. Kolek, and RM du Bois. "Chemokine Network in Pulmonary Sarcoidosis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3186.

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Mei, JunJie, Ning Dai, Yuhong Liu, Samithamby Jeyaseelan, Susan H. Guttentag, Janet S. Lee, and G. Scott Worthen. "Bacterial Pneumonia And Chemokine Clearance." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a6110.

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Chen, Huanhuan, Serena Tucci, Zeynep Gümüs, Xiling Shen, and Steven M. Lipkin. "Abstract 5207: The chemokine 25 and chemokine receptor 9 axis suppresses colon cancer invasion and metastasis." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5207.

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Malki, Mohammed Imad. "Contribution of Glycosaminoglycan binding in CCL21-mediated Migration of Breast Cancer cells." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0081.

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Lymph node metastasis constitutes a key event in Breast Cancer progression and it is a process at least partially mediated by the chemokine CCR7. Chemokine function is dependent upon their binding to both cell-surface glycosaminoglycans (GAGs) molecules and to their specific receptors; thus, the role of GAGs in CCR7-mediated lymph node metastasis was investigated by creating a non-GAG binding chemokine CCL21 (mut-CCL21). Mut-CCL21 (Δ98-134) was synthesized, at 50nM it had similar potential to mobilize intracellular calcium compared to wild-type CCL21 (WT-CCL21). Next, a series of experiments was performed to determine how deletion of the GAG-binding site altered the ability of CCL21 to stimulate chemotaxis within a concentration gradient generated by free solute diffusion. Both WT-CCL21 and mut-CCL21 had a similar potential to stimulate chemotactic migration of PBMC (P>0.05). However, 4T1-Luc cells exhibit reduced migration at 30 & 50nM (p<0.001). Interestingly, this effect was greatly exacerbated in trans-endothelial migration, with the mut-CCL21 failing to increase cell migration above the background level at 30 nM in PBMC and 4T1-Luc cells (p> 0.001 vs WT). This difference could potentially be attributed to reduced GAG binding, as surface plasmon resonance spectroscopy showed that mut-CCL21 did not significantly bind heparan sulphate compared to the WT-CCL21. Finally, a murine model was used to assess the potential of mut-CCL21 to prevent lymph node metastasis in vivo. Mice were injected with 4T1-Luc cells in the mammary fat pad and treated daily for a week with 20µg mut-CCL21 once the tumor was visible. Mice were imaged weekly with IVIS to assess bioluminescence and sacrificed on day 18. Luciferase expression was significantly reduced in lymph nodes from mice that had been treated with mut-CCL21 compared to the control (p=0.0148), suggesting the potential to target chemokine binding to GAGs as a therapeutic option.
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Zavitz, CC, GJ Gaschler, CM Bauer, KM Fraser, and MR Stampfli. "Chemokine Dysregulation in Heterologous Viral-Bacterial Infection." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a3254.

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Kidd, LaCreis R., Sydney C. Beache, Jie Zheng, Guy Brock, James W. Lillard, James Rudd, and Kevin S. Kimbro. "Abstract 2780: Chemokine and chemokine receptor genetic variants as predictors of aggressive prostate cancer among European-American men." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2780.

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Ghanbar, M. I., A. F. Villabona-Rueda, F. R. D'Alessio, and K. Suresh. "Programmed Cell Death Protein-1 Receptor Modulates Chemokine Ligand-18 Secretion in Macrophages: An Important Checkpoint Inhibitor Pneumonitis Chemokine." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a4828.

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Costa, Leonardo, Jürgen Haas, Henriette Rudolph, Saskia Libicher, Sven Jarius, Tobias Tenenbaum, Horst Schroten, and Brigitte Brigitte Wildemann. "The Choroid Plexus Is Permissive for a Preactivated Antigen-Experienced Memory B Cell Subset in Multiple Sclerosis." In Building Bridges in Medical Science 2021. Cambridge Medicine Journal, 2021. http://dx.doi.org/10.7244/cmj.2021.03.001.2.

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Background: The role of B cells in multiple sclerosis (MS) is increasingly recognized. B cells undergo compartmentalized redistribution in blood and cerebrospinal fluid (CSF) during active MS, whereby memory B cells accumulate in the CSF. While B-cell trafficking across the blood– brain barrier has been intensely investigated, cellular diapedesis through the blood–CSF barrier (BCSFB) is incompletely understood. Objectives: To investigate how B cells interact with the choroid plexus to transmigrate into the CSF, we isolated circulating B cells from healthy donors (HC) and MS patients, utilized an inverted cell culture filter system of human choroid plexus papilloma (HIBCPP) cells to determine transmigration rates of B-cell subsets, immunofluorescence, and electron microscopy to analyze migration routes, and qRT-PCR to determine cytokines/chemokines mediating B-cell diapedesis. We also screened the transcriptome of intrathecal B cells from MS patients. Results: We found that spontaneous transmigration of HC- and MS-derived B cells was scant yet increased significantly in response to B-cell specific chemokines CXCL-12/CXCL-13, was further boosted upon pre-activation and occurred via paracellular and transcellular pathways. Migrating cells exhibited upregulation of several genes involved in B-cell activation/migration and enhanced expression of chemokine receptors CXCR4/CXCR5 and were predominantly of isotype class switched memory phenotype. This antigen-experienced migratory subset displayed more pronounced chemotactic activities in MS than in HC and was retrieved in intrathecal B cells from patients with active MS. Trafficking of class-switched memory B cells was downscaled in a small cohort of natalizumab-exposed MS patients and the proportions of these phenotypes were reduced in peripheral blood yet were enriched intrathecally in patients who experienced recurrence of disease activity after withdrawal of natalizumab. Conclusion: Our findings highlight the relevance of the BCSFB as an important gate for the entry of potentially harmful activated B cells into the CSF.
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Du, X., F. Li, N. Li, Z. Shao, C. Zhang, H. Huang, W. Li, Z. Chen, S. Ying, and H. Shen. "Eosinophil-Derived Chemokine CCL6 Promote Allergic Airway Inflammation." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7630.

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Reports on the topic "Chemokine"

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Zou, Chenghui, Weng Zhang, Mao Li, Dan He, Yujie Han, and Mao Lu. A meta-analysis of association between CCL5、CCL11、CCL17 polymorphisms and AD. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0148.

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Review question / Objective: At present, many studies on the association between CCL5、CCL11、CCL17 polymorphisms and atopic dermatitis（AD）are inconsistent. We conducted this meta-analysis of Case control trial to evaluate the association between CCL5、CCL11、CCL17 polymorphisms and atopic dermatitis（AD). Condition being studied: Since the discovery of cytokines, and in particular the role of chemokines in the progression of AD, many clinical studies have been carried out around the world to explore the association of AD with chemokine polymorphism. However, the quality, type and conclusions of studies on the correlation between chemokine polymorphism and AD are inconsistent. Foreign studies have shown that chemokine polymorphism is statistically significant in relation to AD. Studies by Menzies-Gow A et al have shown that a new therapeutic strategy targeting to block CCL11 signal has been proven to significantly improve patients with moderate to severe AD. However, some foreign studies have also reported that chemokine polymorphism is unrelated to AD.
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Reshef, Ran. Chemokine Receptor Signatures in Allogeneic Stem Cell Transplantation. Fort Belvoir, VA: Defense Technical Information Center, August 2014. http://dx.doi.org/10.21236/ada610688.

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McCarthy, James B. Chemokine Receptors and Integrin Function in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2002. http://dx.doi.org/10.21236/ada412790.

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McCarthy, James B. Chemokine Receptors and Integrin Function in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, February 2000. http://dx.doi.org/10.21236/ada391087.

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Shurin, Michael R. Epigenetic Regulation of Chemokine Expression in Prostate Cancer. Fort Belvoir, VA: Defense Technical Information Center, December 2006. http://dx.doi.org/10.21236/ada460756.

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Reshef, Ran. Chemokine Receptor Signatures in Allogeneic Stem Cell Transplantation. Fort Belvoir, VA: Defense Technical Information Center, August 2015. http://dx.doi.org/10.21236/ada620593.

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Symons, Marc H. Role of Rac GTPases in Chemokine-Stimulated Breast Carcinoma. Fort Belvoir, VA: Defense Technical Information Center, July 2006. http://dx.doi.org/10.21236/ada457469.

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Symons, Marc. Role of Rac GTPases in Chemokine-Stimulated Breast Carcinoma Metastasis. Fort Belvoir, VA: Defense Technical Information Center, January 2009. http://dx.doi.org/10.21236/ada502287.

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Symons, Marc. Role of Rac GTPasas in Chemokine-Stimulated Breast Carcinoma Metastasis. Fort Belvoir, VA: Defense Technical Information Center, July 2007. http://dx.doi.org/10.21236/ada473355.

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Murphy, William J. Chemokine Blockade in Combination with Cytoreductive Conditioning in Metastatic Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, August 2006. http://dx.doi.org/10.21236/ada466180.

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