Relevant bibliographies by topics / Chemokines

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Chemokines'

Author: Grafiati
Published: 4 June 2021
Last updated: 2 November 2024

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Journal articles on the topic "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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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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Dissertations / Theses on the topic "Chemokines"

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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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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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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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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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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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Simmons, Graham. "Human immunodeficiency syndrome virus type 1 cell tropism and inhibition by chemokines and chemokine analogues." Thesis, Institute of Cancer Research (University Of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.368041.

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Juremalm, Mikael. "The Role of Chemokines in Mast Cell Migration." Doctoral thesis, Uppsala University, Department of Genetics and Pathology, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3273.

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Mast cells are very potent multifunctional effector cells of the immune system normally distributed throughout connective tissues. An accumulation of mast cells has been described in several pathological conditions such as allergic- and autoimmune inflammations and in certain tumours. This necessitates two different processes: 1) Recruitment of mast cell progenitors from peripheral blood; 2) Accretion of mature mast cells at sites of inflammation and tumour areas. Both processes are depending on the local production of chemotactic factors. The aim of this study was to investigate the role of chemokines and their corresponding receptors in mast cell chemotaxis.

By cloning and mRNA-screening of cord blood derived mast cells several chemokine receptors were found to be expressed. Functional expression was confirmed of chemokine receptors CXCR4, CCR1 and CCR4. CXCL12, the only known ligand for CXCR4, acted as a mast cell chemotaxin and induced migration of progenitor cells with capacity to differentiate into mast cells. Of several ligands known to bind CCR1 and CCR4, only CCL5 induced migration of mast cells. The migration to CCL5 was mediated through both CCR1 and CCR4. In contrast, the ligands to CCR4, CCL17 and CCL22, could inhibit CCL5-induced migration. Expression of CCR1 and CCR4 could also be confirmed on mast cells in lung from asthmatic patients. Furthermore, we could demonstrate that mast cells were attracted by CCL5 produced by tumour cells in Hodgkin´s lymphoma.

In conclusion, the work in this thesis has identified two chemokines that regulates mast cell migration. This knowledge helps us understand the mechanisms behind homing of mast cell progenitors from the blood into the tissue and the accumulation of mature mast cells at sites of inflammation and tumourigenesis.

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Books on the topic "Chemokines"

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M, Schwiebert Lisa, ed. Chemokines, chemokine receptors, and disease. Amsterdam: Elsevier Academic, 2005.

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Cardona, Astrid E., and Eroboghene E. Ubogu, eds. Chemokines. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-426-5.

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Tschammer, Nuska, ed. Chemokines. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-14060-5.

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service), ScienceDirect (Online, ed. Chemokines. London: Academic, 2009.

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E, Kownatzki, and Norgauer J, eds. Chemokines and skin. Basel: Birkhauser Verlag, 1998.

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Ubogu, Eroboghene E., and Astrid E. Cardona. Chemokines: Methods and protocols. New York: Humana Press, 2013.

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Lindley, I. J. D., J. Westwick, and S. Kunkel, eds. The Chemokines. Boston, MA: Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2952-1.

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Rollins, Barrett J., ed. Chemokines and Cancer. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-701-7.

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Hébert, Caroline A., ed. Chemokines in Disease. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-706-2.

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Kownatzki, Eckhard, and Johannes Norgauer, eds. Chemokines and Skin. Basel: Birkhäuser Basel, 1998. http://dx.doi.org/10.1007/978-3-0348-8843-1.

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Book chapters on the topic "Chemokines"

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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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Lira, Sergio A., Paul J. Zavodny, and Daniel Lundell. "Chemokines." In New Cytokines as Potential Drugs, 121–38. Basel: Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8456-3_8.

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Barnette, M. S., and R. Schleimer. "Chemokines." In Therapeutic Strategies for Modulating the Inflammatory Diseases, 95–97. Basel: Birkhäuser Basel, 1998. http://dx.doi.org/10.1007/978-3-0348-8857-8_17.

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Teran, Luis M., and Juan R. Velazquez. "Chemokines." In Inflammation and Allergy Drug Design, 253–61. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444346688.ch20.

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Fang, Lei, and Sam T. Hwang. "Chemokines." In Encyclopedia of Cancer, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_1066-4.

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Eugenin, Eliseo A., and Joan W. Berman. "Chemokines." In Encyclopedia of Medical Immunology, 279–86. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-0-387-84828-0_34.

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Fernandez-Botran, Rafael. "Chemokines." In Encyclopedia of Immunotoxicology, 171–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_248.

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Kalmar, Jayne M., Brigid M. Lynch, Christine M. Friedenreich, Lee W. Jones, A. N. Bosch, Alessandro Blandino, Elisabetta Toso, et al. "Chemokines." In Encyclopedia of Exercise Medicine in Health and Disease, 180. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2221.

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Conference papers on the topic "Chemokines"

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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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Dahmardeh, Mahyar, Houman Mirzaalian Dastjerdi, Hisham Mazal, Harald Köstler, and Vahid Sandoghdar. "Breaking new ground in protein detection: Self-supervised machine learning and iSCAT enable label-free detection of single proteins below 10 kDa." In Bio-Optics: Design and Application. Washington, D.C.: Optica Publishing Group, 2023. http://dx.doi.org/10.1364/boda.2023.jw2a.3.

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Interferometric scattering (iSCAT) microscopy detects single nanoparticles in a label-free fashion. Utilizing self-supervised machine learning pushes the detection sensitivity of iSCAT to very small proteins and disease markers such as chemokines and cytokines.
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Strieter, Robert. "Abstract ED03-03: CXC chemokines in cancer." In Abstracts: Frontiers in Cancer Prevention Research 2008. American Association for Cancer Research, 2008. http://dx.doi.org/10.1158/1940-6207.prev-08-ed03-03.

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Schneider, Dina, Deepti R. Nagarkar, Emily R. Bowman, Christina L. McHenry, Marisa J. Linn, Adam M. Goldsmith, Babina Gosangi, John K. Bentley, Toby C. Lewis, and Marc B. Hershenson. "CC Chemokines And RV-Induced Asthma Exacerbations." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4226.

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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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Drösslerová, Marie, Martina Šterclová, Martina Vašáková, Alice Tašková, Vladislav Hytych, Eva Richterová, and Milada Matějčková. "Role of chemokines, their gene polymorphisms in resectable NSCLC." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.4094.

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Jung, Yun Jung, Wou Young Chung, Keu Sung Lee, Seung Soo Sheen, Joo Hun Park, and Kwang Joo Park. "Significance of interferon gamma-inducible chemokines in pleural effusions." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa4521.

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Mahgoub, Yasmine, Rida Arif, and Susu Zughaier. "Pyocyanin pigment from Pseudomonas aeruginosa modulates innate immune defenses in macrophages." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0137.

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Background: Pseudomonas aeruginosa is a well-known opportunistic pathogen. The gram-negative bacillus, commonly associated with hospital-acquired infections, utilizes the host’s impaired immune responses to establish infection. Of its many virulence factors, pyocyanin is essential for P. aeruginosa to establish its full infectivity. Macrophages act as sentinels of the innate immune system, as well as play other roles in homeostasis, tissue remodeling, and bridging between the innate and adaptive immune systems. Aim: This study aimed to investigate the effects of pyocyanin on macrophage innate immune defenses by assessing the function of macrophages treated with pyocyanin and TLR ligands. Phagocytosis of opsonized zymosan, LPS-induced nitric oxide release and cytokine release were used as measures of functional responses. Results: This study found that pyocyanin inhibited phagocytosis-induced ROS release in a dose-dependent manner and reduced nitric oxide release from macrophages induced with P. aeruginosa LPS. In addition, pyocyanin modulated cytokines and chemokines release from macrophages exposed to P. aeruginosa LPS in a dose-dependent manner. Pyocyanin significantly enhanced IL-1β release as well as several chemokines. Therefore, pyocyanin facilitates Pseudomonas aeruginosa to persevere in the immunocompromised host through modulating macrophage’s innate immune defenses. Conclusion: Pyocyanin inhibits macrophage functional defense responses to facilitate Pseudomonas aeruginosa infection.
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Zhen, LI, Huiqin Hao, Ze Wang, Wenjing Lu, and Yang Liu. "AB0121 EXPRESSION OF CHEMOKINES AND CHEMOKINE RECEPTORS IN DIFFERENT TISSUES AND THEIR LOCALIZATION IN THE JOINTS OF RATS WITH RHEUMATOID ARTHRITIS." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.5189.

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Korchynskyi, Olexandr. "SAT0053 GLYCOSYLATION IN MAMMALS PROTECTS CITRULLINATED CHEMOKINES FROM PARTIAL DEGRADATION." In Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.8072.

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Reports on the topic "Chemokines"

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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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Fox, David A. Citrullinated Chemokines in Rheumatoid Arthritis. Fort Belvoir, VA: Defense Technical Information Center, October 2014. http://dx.doi.org/10.21236/ada611994.

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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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