Relevant bibliographies by topics / Chemokine biology

Academic literature on the topic 'Chemokine biology'

Author: Grafiati
Published: 10 December 2022
Last updated: 28 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Chemokine biology.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Chemokine biology"

1

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

Full text
Abstract:
The chemokines are a complex superfamily of small, secreted proteins that were initially characterized through their chemotactic effects on a variety of leucocytes. The superfamily is divided into families based on structural and genetic considerations and have been termed the CXC, CC, C and CX3C families. Chemokines from these families have a key role in the recruitment and function of T lymphocytes. Moreover, T lymphocytes have also been identified as a source of a number of chemokines. T lymphocytes also express most of the known CXC and CC chemokine receptors to an extent that depends on their state of activation/differentiation and/or the activating stimuli. The expression of two chemokine receptors, namely CXCR4 and CCR5, together with the regulated production of their respective ligands, appears to be extremely important in determining sensitivity of T cells to HIV-1 infection. The intracellular events which mediate the effects of chemokines, particularly those elicited by the CC chemokine RANTES, include activation of both G-protein- and protein tyrosine kinase-coupled signalling pathways. The present review describes our current understanding of the structure and expression of chemokines and their receptors, the effects of chemokines on T-cell function(s), the intracellular signalling pathways activated by chemokines and the role of certain chemokines and chemokine receptors in determining sensitivity to HIV-1 infection.
APA, Harvard, Vancouver, ISO, and other styles
2

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
3

Liu, Dongxiang, Navid Madani, Ying Li, Rong Cao, Won-Tak Choi, Sameer P. Kawatkar, Mi Youn Lim, et al. "Crystal Structure and Structural Mechanism of a Novel Anti-Human Immunodeficiency Virus and d-Amino Acid-Containing Chemokine." Journal of Virology 81, no. 20 (August 8, 2007): 11489–98. http://dx.doi.org/10.1128/jvi.02845-06.

Full text
Abstract:
ABSTRACT Chemokines and their receptors play important roles in normal physiological functions and the pathogeneses of a wide range of human diseases, including the entry of human immunodeficiency virus type 1 (HIV-1). However, the use of natural chemokines to probe receptor biology or to develop therapeutic drugs is limited by their lack of selectivity and the poor understanding of mechanisms in ligand-receptor recognition. We addressed these issues by combining chemical and structural biology in research into molecular recognition and inhibitor design. Specifically, the concepts of chemical biology were used to develop synthetically and modularly modified (SMM) chemokines that are unnatural and yet have properties improved over those of natural chemokines in terms of receptor selectivity, affinity, and the ability to explore receptor functions. This was followed by using structural biology to determine the structural basis for synthetically perturbed ligand-receptor selectivity. As a proof-of-principle for this combined chemical and structural-biology approach, we report a novel d-amino acid-containing SMM-chemokine designed based on the natural chemokine called viral macrophage inflammatory protein II (vMIP-II). The incorporation of unnatural d-amino acids enhanced the affinity of this molecule for CXCR4 but significantly diminished that for CCR5 or CCR2, thus yielding much more selective recognition of CXCR4 than wild-type vMIP-II. This d-amino acid-containing chemokine also showed more potent and specific inhibitory activity against HIV-1 entry via CXCR4 than natural chemokines. Furthermore, the high-resolution crystal structure of this d-amino acid-containing chemokine and a molecular-modeling study of its complex with CXCR4 provided the structure-based mechanism for the selective interaction between the ligand and chemokine receptors and the potent anti-HIV activity of d-amino acid-containing chemokines.
APA, Harvard, Vancouver, ISO, and other styles
4

Kelvin, David J., Dennis F. Michiel, James A. Johnston, Andrew R. Lloyd, Hans Sprenger, Joost J. Oppenheim, and Ji-Ming Wang. "Chemokines and serpentines: the molecular biology of chemokine receptors." Journal of Leukocyte Biology 54, no. 6 (December 1993): 604–12. http://dx.doi.org/10.1002/jlb.54.6.604.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Borroni, Elena M., Raffaella Bonecchi, and Annalisa M. VanHook. "Science Signaling Podcast: 30 April 2013." Science Signaling 6, no. 273 (April 30, 2013): pc11. http://dx.doi.org/10.1126/scisignal.2004231.

Full text
Abstract:
This Podcast features an interview with Elena M. Borroni and Raffaella Bonecchi, authors of a Research Article that appears in the 30 April 2013 issue of Science Signaling. Chemokines recruit leukocytes to sites of infection and inflammation by binding to chemokine receptors, which are members of the G protein–coupled receptor superfamily, present on the surface of leukocytes. Whereas activation of typical chemokine receptors leads to G protein–dependent signaling that promotes cell migration toward the chemokine source, activation of atypical chemokine receptors does not promote cell migration. Instead, signaling initiated by atypical chemokine receptors contributes to the immune response in other ways. The atypical chemokine receptor D6 is a scavenger that alters the chemokine gradient by binding to and degrading chemokines. Borroni and Bonecchi found that activation of a β-arrestin–dependent signaling pathway was necessary for D6 to act as a chemokine scavenger.
APA, Harvard, Vancouver, ISO, and other styles
6

Caligiuri, Alessandra, Mirella Pastore, Giulia Lori, Chiara Raggi, Giovanni Di Maira, Fabio Marra, and Alessandra Gentilini. "Role of Chemokines in the Biology of Cholangiocarcinoma." Cancers 12, no. 8 (August 7, 2020): 2215. http://dx.doi.org/10.3390/cancers12082215.

Full text
Abstract:
Cholangiocarcinoma (CCA), a heterogeneous tumor with poor prognosis, can arise at any level in the biliary tree. It may derive from epithelial cells in the biliary tracts and peribiliary glands and possibly from progenitor cells or even hepatocytes. Several risk factors are responsible for CCA onset, however an inflammatory milieu nearby the biliary tree represents the most common condition favoring CCA development. Chemokines play a key role in driving the immunological response upon liver injury and may sustain tumor initiation and development. Chemokine receptor-dependent pathways influence the interplay among various cellular components, resulting in remodeling of the hepatic microenvironment towards a pro-inflammatory, pro-fibrogenic, pro-angiogenic and pre-neoplastic setting. Moreover, once tumor develops, chemokine signaling may influence its progression. Here we review the role of chemokines in the regulation of CCA development and progression, and the modulation of angiogenesis, metastasis and immune control. The potential role of chemokines and their receptors as possible biomarkers and/or therapeutic targets for hepatobiliary cancer is also discussed.
APA, Harvard, Vancouver, ISO, and other styles
7

Gustavsson, Martin, Douglas P. Dyer, Chunxia Zhao, and Tracy M. Handel. "Kinetics of CXCL12 binding to atypical chemokine receptor 3 reveal a role for the receptor N terminus in chemokine binding." Science Signaling 12, no. 598 (September 10, 2019): eaaw3657. http://dx.doi.org/10.1126/scisignal.aaw3657.

Full text
Abstract:
Chemokines bind to membrane-spanning chemokine receptors, which signal through G proteins and promote cell migration. However, atypical chemokine receptor 3 (ACKR3) does not appear to couple to G proteins, and instead of directly promoting cell migration, it regulates the extracellular concentration of chemokines that it shares with the G protein–coupled receptors (GPCRs) CXCR3 and CXCR4, thereby influencing the responses of these receptors. Understanding how these receptors bind their ligands is important for understanding these different processes. Here, we applied association and dissociation kinetic measurements coupled to β-arrestin recruitment assays to investigate ACKR3:chemokine interactions. Our results showed that CXCL12 binding is unusually slow and driven by the interplay between multiple binding epitopes. We also found that the amino terminus of the receptor played a key role in chemokine binding and activation by preventing chemokine dissociation. It was thought that chemokines initially bind receptors through interactions between the globular domain of the chemokine and the receptor amino terminus, which then guides the chemokine amino terminus into the transmembrane pocket of the receptor to initiate signaling. On the basis of our kinetic data, we propose an alternative mechanism in which the amino terminus of the chemokine initially forms interactions with the extracellular loops and transmembrane pocket of the receptor, which is followed by the receptor amino terminus wrapping around the core of the chemokine to prolong its residence time. These data provide insight into how ACKR3 competes and cooperates with canonical GPCRs in its function as a scavenger receptor.
APA, Harvard, Vancouver, ISO, and other styles
8

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

Full text
Abstract:
Abstract Chemokine receptors play important roles in many physiological processes and are implicated in a wide range of human diseases including acute respiratory distress syndrome, allergic asthma, psoriasis, arthritis, multiple sclerosis, cancer, atherosclerosis and most notably AIDS. To enable the applications of chemokine ligands as probes of receptor biology and pharmacology, and inhibitors of diseases mediated by chemokine receptors, a major problem with the lack of receptor selectivity of these natural chemokines must be overcome. In this study, we have developed a chemical approach combining total protein synthesis and modular modifications to generate a new family of unnatural chemokines termed SMM-chemokines (which refer to synthetically and modularly modified chemokines) with designed receptor selectivity and affinity. A proof of the concept has been provided by applying this strategy to transform a very nonselective chemokine vMIP-II into new analogs with enhanced selectivity and potency for CXCR4 or CCR5, two principal coreceptors for HIV-1 entry. Such novel molecules have been shown subsequently to be valuable probes in gaining insights into receptor binding and signaling mechanisms, and as potent inhibitors to prevent HIV-1 entry and infection. These results strongly support the design concept of these SMM-chemokines and suggest that general applicability of this approach for studying and controlling other chemokine receptors and the diseases they mediate might be anticipated.
APA, Harvard, Vancouver, ISO, and other styles
9

Balkwill, Fran. "Chemokine biology in cancer." Seminars in Immunology 15, no. 1 (February 2003): 49–55. http://dx.doi.org/10.1016/s1044-5323(02)00127-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

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.

Full text
Abstract:
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.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Chemokine biology"

1

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.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Millette, Roxanne. "The effect of chemokine CCL19 on B lymphocytes /." Thesis, McGill University, 2002. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=79051.

Full text
Abstract:
B-T lymphocyte interaction within lymphoid tissues following antigen exposure is a crucial step in the generation of high affinity antibody. Due to its expression pattern and specificity for B lymphocytes, CC Chemokine Ligand 19 (CCL19) may help initiate the adaptive humoral immune response following antigen exposure. Here we show CCL 19 induced [Ca2+]i mobilization, chemotaxis and rescue from apoptosis in B lymphocytes. Because CCL19 is constitutively expressed, we studied the expression and signalling properties of its corresponding chemokine receptor, CC chemokine receptor 7 (CCR7) in various B cell populations. We found that CCL19 responsive CCR7 + cells belonged to distinct B lymphocyte populations at particular stages of maturation and that BCR crosslinking alone was insufficient to modulate CCR7 expression and CCL19 responsiveness. CCL19 induced signal transduction events were Galphai dependent. We found that CCL19 stimulation could desensitize the CCR7 receptor to further CCL19 stimulation, but did not interfere with other key B cell activation signals such as BCR and PAF. Our results implicate CCL19 in B lymphocyte activation, migration, and survival.
APA, Harvard, Vancouver, ISO, and other styles
3

Finley, Matthew James. "Molecular Basis for Kappa-Opioid Regulation of Chemokine Receptor Function." Diss., Temple University Libraries, 2009. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/62878.

Full text
Abstract:
Molecular Biology and Genetics
Ph.D.
Opioid receptor-mediated regulation of chemokine receptors is vital for the host immune response, development, and neurological function. Previous studies have demonstrated that the kappa opioid receptor (KOR) activation results in decreased infectivity of human immunodeficiency virus 1 (HIV-1) in human peripheral blood mononuclear cells (PBMCs). We have found this effect is due to down-regulation of the major HIV-1 co-receptors, CCR5 and CXCR4. Using molecular techniques, CCR5 and CXCR4 mRNA levels drop dramatically following KOR activation. To dissect the mechanism involved, we used transcription factor binding arrays and compared control cell extracts to KOR activated cell extracts. We determined that the interferon regulatory factors (IRFs) and signal transducers and activators of transcription (STATs) could be involved in the KOR-mediated repression of CCR5 and CXCR4 transcription and protein expression. Using chemical inhibitors and small interfering RNA (siRNA) molecules, we determined that JAK2, STAT3, and IRF2 are critical members of this signal transduction pathway. The understanding of these particular mechanisms should prove to be beneficial for the development of potential pharmacological agents targeted at HIV-1 binding and infection since virus infection requires expression of the co-receptors CXCR4 and CCR5. Understanding the molecular basis for KOR-induced inhibition of co-receptor expression may provide a basis for the development of KOR agonist-based therapeutics to treat individuals infected with HIV.
Temple University--Theses
APA, Harvard, Vancouver, ISO, and other styles
4

Zhu, John Z. "Sulfotyrosines impart ligand specificity in a chemokine receptor model system." [Bloomington, Ind.] : Indiana University, 2009. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3380144.

Full text
Abstract:
Thesis (Ph.D.)--Indiana University, Dept. of Biochemistry, 2009.
Title from PDF t.p. (viewed on Jul 20, 2010). Source: Dissertation Abstracts International, Volume: 70-12, Section: B, page: 7377. Advisers: Martin J. Stone; Carl E. Bauer.
APA, Harvard, Vancouver, ISO, and other styles
5

Tiplady, Eleanor Margaret. "Expression and modulation of atypical chemokine receptors on epithelial cells." Thesis, University of Glasgow, 2018. http://theses.gla.ac.uk/30618/.

Full text
Abstract:
The immune system relies on the correct spatial and temporal positioning of cells in order to function; cells need to be able to move throughout the circulatory system to survey for pathogens, to migrate from their resident sites in tissues when they sense infection or injury to alert other cells, or to migrate to the site of damage or infection to help mobilise a response. These functions often involve chemokines, small cytokines that signal through chemokine receptors, which are G-protein coupled receptors expressed on the cell membrane. Different chemokines are regulated differentially and can be associated with certain tissues or developmental processes, meaning the suite of receptors expressed by each cell type determines which tissues it is capable of entering, and the precise location it takes up once inside the tissue. Atypical chemokine receptors are a class of chemokine receptors that do not initiate the downstream signalling pathways typical of a G-protein coupled receptor, as they do not recruit intracellular G-proteins, and generally don't induce cell migration. Instead, these receptors are thought to function mainly as chemokine scavenging receptors, internalising and destroying their ligands before rapidly recycling to the cell surface. In this way, the levels of chemokines in the body are prevented from becoming oversaturated thus dampening the ability of cells to respond to signals. ACKR3 and ACKR4 are two atypical chemokine receptors that are expressed on endothelial cells and keratinocytes in the skin. Here, I have studied their expression on cultured human lymphatic endothelial cells and keratinocytes, and modulation in response to immune stimuli on these cells using a combination of qPCR and immunofluorescent staining. These strategies revealed that ACKR3 and ACKR4 are expressed on cultured LECs and keratinocytes and may be differentially regulated by both cell types in response to inflammatory stimuli including bacterial (LPS) and viral (Unmethylated CpG DNA) signatures. Although chemokine scavenging activity could not be detected on these cells, these findings suggested a role for ACKRs 3 and 4 in the inflammatory response. Further experiments in vivo explored the expression and modulation of ACKR3/CXCR4 and ACKR4 on epithelial cells including lymphatic endothelial cells, keratinocytes and vascular endothelial cells in the spleen. Flow cytometry was used to examine tissues both at rest and after inflammation (Aldara-mediated psoriasis model, or TPA-mediated contact hypersensitivity model) and investigate the regulation of ACKR3/CXCR4 or ACKR4 in response to these stimuli. Key findings included the strong overlap and differential regulation of ACKR3 and CXCR4 in response to TPA in the infundibulum subset of keratinocytes. Additionally, lymph nodes of Ackr4-/- mice were significantly enlarged after repeated treatments with Aldara. This appeared to be due to CCL19 dysregulation, but adoptive transfer suggested that there was no defect in leukocyte homing in these mice. This suggested an as yet undetermined response to enhanced CCL19 bioavailability that did not prevent the correct migration of leukocytes to secondary lymphoid organs. Overall, these experiments suggested that ACKR3 and ACKR4 are modulated in response to several inflammatory stimuli both in vivo and in vitro, and that the modulation of homeostatic chemokines can play a role in the response to inflammatory events. This was particularly important in the context of skin inflammation, where inflammatory chemokines, CXCR4 and ACKR2 have all been implicated in severity and duration of inflammatory events, but few studies have yet described the potential contributions of ACKR3 or ACKR4.
APA, Harvard, Vancouver, ISO, and other styles
6

Randolph-Habecker, Julie. "The expression and function of the human cytomegalovirus encoded beta-chemokine receptor homolog, US28 /." The Ohio State University, 1998. http://rave.ohiolink.edu/etdc/view?acc_num=osu148795159550182.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Cook, Sarah Louise. "The role of CC-chemokine receptor-like 2 in the B cell response." Thesis, University of Birmingham, 2015. http://etheses.bham.ac.uk//id/eprint/5645/.

Full text
Abstract:
CCRL2 is a member of the atypical chemattractant family. It has been proposed to bind the chemokines CCL19 and CCL5, as well as the adipokine chemerin. Unlike typical chemokine receptors, atypical chemoattractant receptors do not undergo conventional G protein signalling upon binding, but instead degrade, transcytose or present their ligands on the cell surface. This study aims to characterise the role of CCRL2 in B cells upon their activation and differentiation into either extrafollicular plasmablasts or germinal centre B cells. CCRL2 mRNA is upregulated upon plasmablast differentiation. Upon immunisation with NP-Ficoll, CCRL2 deficient mice produce more NP-specific antibody and larger numbers of NP-specific plasmablasts. Further assessment show this phenotype is due to B cell intrinsic effects. CCRL2 deficient plasmablasts tend to proliferate more and undergo less apoptosis than CCRL2 expressing plasmablasts. The role of CCRL2 in the germinal centre was also assessed. Germinal centres formed normally, including polarisation into light and dark zones in CCRL2 deficient mice. However, FDCs within the germinal centre appeared to extend further into the follicular mantle in CCRL2 deficient mice. This may be the cause of an increased proportion of germinal centres over the whole spleen in CCRL2 deficient mice. These differences did not result in significant changes in affinity maturation. Together, this shows a novel role for CCRL2 in the regulation of the extrafollicular plasmablast response to NP-Ficoll. However, minor differences in CCRL2 deficient germinal centres do not affect high affinity plasma cell output, suggesting a minimal role of CCRL2 in GC function.
APA, Harvard, Vancouver, ISO, and other styles
8

Mukhi, Sumedha. "Effects of Chronic Morphine Administration on Cytokine & Chemokine Protein and Gene Expression." Master's thesis, Temple University Libraries, 2012. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/214787.

Full text
Abstract:
Molecular Biology and Genetics
M.S.
Chemokine and chemokine receptors play a major role in HIV-1 infectivity, and their expression can be modulated by opioid drugs of abuse, further implicating a role for these drugs in altering HIV-1 susceptibility. Several of the opioid agonists including morphine and heroin impair resistance to a variety of infectious agents including HIV-1 by modulating both innate and acquired immune responses. The aim of my thesis is to understand whether chronic morphine administration alters the expression of pro-inflammatory cytokines and chemokines. Since there are limited reports in the literature describing the effects of chronic opioid administration on immune competence, a macaque model was devised to analyze the immune system following chronic morphine administration. My results show that animals receiving morphine exhibit enhanced proinflammatory CXCL8 protein expression in response to stimulation with various Toll Receptor (TLR) ligands. This result was observed in responses to either the combination of LPS and IFNγ, or with the TLR ligand peptidoglycan. These results suggest that chronic morphine administration increases immune system responsiveness. We extended these studies on opioid-induced signaling and gene expression in human subjects and observed that opioid treatment induces the expression of CXCL10, TLR4, and the aryl hydrocarbon receptor (AHR) in leukocytes early in response to treatment. In sum, I have shown that opioid agonists modulate important immune-response genes, and these genes are important for the generation of antimicrobial immunity.
Temple University--Theses
APA, Harvard, Vancouver, ISO, and other styles
9

Jung, Jaeho. "Cytokine and chemokine gene expression during influenza virus infection, and the effects of restraint stress /." The Ohio State University, 1996. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487942182322557.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Qu, Yiding. "Role of non-signaling (decoy) chemokine receptors in regulating cell migration: the mathematical model." Thesis, McGill University, 2013. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=114337.

Full text
Abstract:
Chemokines belong to a family of important chemoattractants that guide the directional migration of the cell. The cognate chemokine receptor on the cell senses the chemokine gradient and the cell moves towards the signal of increasing chemokine concentration. However, several chemokine receptors were recently identified as non-signaling (decoy), based on their ability to bind the chemokine but produce no measurable signal for the cell. The function of these decoy receptors is yet unknown. We hypothesized that the ligand binding by the decoy receptor may help maintaining a sharper chemokine gradient and thus stimulate the cell migration. We first assessed if the expression of decoy and corresponding signaling receptors changes when cancer cells acquire migratory phenotype – become metastatic. Using publically available database of gene expression in normal prostate, carcinoma and metastatic prostate cancer samples, we have found that the expression of decoy receptors CCX-CKR and OPG increased in metastatic cancer cells compared to normal prostate and positively correlated with the expression of signaling receptors CCR7 and RANK respectively. We next developed mathematical model that described the dynamics of chemokine ligand, normal receptor and decoy receptor as well as subsequent cell movement. Using this model we first assessed how the cells expressing signaling receptors only migrate towards the source of ligand given at different concentrations. At low levels of ligand, cell migration increased with the increase in ligand concentration. However, at higher concentrations, when the ligand levels exceeded the signaling receptor capacity, further increase in ligand resulted in the decrease the distance of cell migration. Importantly, at high levels of ligand the presence of the decoy receptor improved the speed and distance of cell migration. This study suggests the novel function for the non-signaling chemokine receptors in maintaining the chemokine gradient and positively regulating directional cell migration.
Les chimiokines appartiennent à une importante famille de ligands chimiotactiques qui guident la direction migratoire des cellules. Sur une cellule-cible, des récepteurs spécifiques à une chimiokine donnée répondent à un gradient du ligand, provoquant la migration cellulaire vers le signal avec une concentration croissante. Cependant, quelques récepteurs pouvant liés des chimiokines ont récemment été identifiés comme muets (leurre) parce que la liaison du ligand ne stimule pas de signalisation mesurable dans la cellule. La fonction de ces récepteurs-leurres n'est pas connue actuellement.Nous avons émis l'hypothèse que l'interaction des chimiokines à ces récepteurs-leurres contribue à maintenir un gradient de ligand plus prononcé et donc stimule les cellules à migrer. Afin de tester cette hypothèse, nous avons en premier comparé l'expression de récepteurs signalant et de récepteurs-leurres pour un même ligand, quand des cellules deviennent métastatiques. En utilisant des bases de données publiques sur l'expression des gènes dans des échantillons de prostate normale, de carcinomes prostatiques, et de métastases prostatiques, nous avons remarqué que l'expression des récepteurs-leurres CCX-CKR et OPG est augmentée dans les cellules métastatiques lorsque comparée avec les cellules de prostate normales. Nous avons aussi trouvé une corrélation positive avec les niveaux d'expression des récepteurs signalants CCR7 et RANK. Par la suite, nous avons développé un modèle mathématique qui prédit la dynamique des concentrations de chimiokines, l'expression des récepteurs signalants, des récepteurs-leurres, et des mouvements de la cellule résultants. Nous avons tout d'abord utilisé ce modèle afin de prédire comment des cellules exprimant seulement des récepteurs signalant migrent vers la source du ligand selon sa concentration. En présence de faibles concentrations de ligand, la migration cellulaire augmente proportionnellement à l'augmentation de la concentration du ligand. Cependant, à des concentrations plus élevées dépassant la capacité de liaison du récepteur signalant, une augmentation subséquente diminue la distance migrée par la cellule. L'expression concomittante de récepteurs-leurres améliore la vitesse et la distance de la migration cellulaire lorsque la concentration du ligand est élevée. Cette étude suggère donc que les récepteurs-leurres des chimiokines contribuent au gradient chimiotactique et augmentent la migration des cellules.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Chemokine biology"

1

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Caroline, Hébert, ed. Chemokines in disease: Biology and clinical research. Totowa, N.J: Humana Press, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Neote, Kuldeep, Gordon L. Letts, and Bernhard Moser, eds. Chemokine Biology — Basic Research and Clinical Application. Basel: Birkhäuser Basel, 2007. http://dx.doi.org/10.1007/978-3-7643-7437-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Moser, Bernhard, Gordon L. Letts, and Kuldeep Neote, eds. Chemokine Biology — Basic Research and Clinical Application. Basel: Birkhäuser Basel, 2006. http://dx.doi.org/10.1007/3-7643-7423-3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

International Symposium on Chemotactic Cytokines (2nd 1990 London, England). Chemotacticcytokines: Biology of the inflammatory peptide supergene family. New York: Plenum, 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
6

International Symposium on Chemotactic Cytokines (2nd 1990 London, England). Chemotactic cytokines: Biology of the inflammatory peptide supergene family. New York: Plenum Press, 1991.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
7

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

Find full text
APA, Harvard, Vancouver, ISO, and other styles
8

(Contributor), William W. Agace, Marco Baggiolini (Contributor), Craig T. Morita (Contributor), Federica Sallusto (Contributor), José Miguel Rodriguez-Frade (Contributor), Paul Kubes (Contributor), Basil O. Gerber (Contributor), et al., eds. Chemokine Biology - Basic Research and Clinical Application: Vol. 1: Immunobiology of Chemokines (Progress in Inflammation Research). Birkhäuser Basel, 2005.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

M, Krensky Alan, ed. Biology of the chemokine RANTES. New York: Springer-Verlag, 1995.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
10

Amanda E.I. Proudfoot (Editor), Timothy N.C. Wells (Editor), and Christine Power (Editor), eds. Chemokine Protocols (Methods in Molecular Biology). Humana Press, 2000.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "Chemokine biology"

1

Baird, Anne-Marie, Kenneth J. O’Byrne, and Steven G. Gray. "Epigenetic Regulation of Chemokine/Chemokine Receptor Expression." In Methods in Molecular Biology, 185–201. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-426-5_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Fang, Lei, and Sam T. Hwang. "Roles for CCR7 in Cancer Biology." In Chemokine Receptors in Cancer, 93–108. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-267-4_6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Garin, Alexandre, Zoë Johnson, Aurelie Hermant, Fanny Beltran, Yann Ratinaud, Alexandra Michel, Sonja Krohn, et al. "Chemokine Receptor Antagonist Development." In Methods in Molecular Biology, 67–92. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-426-5_6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Gerard, Craig. "Understanding Chemokine Biology Through Mouse Genetics." In Chemokines in Disease, 41–51. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-706-2_3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Roh, Yoon-Seok, and Ekihiro Seki. "Chemokines and Chemokine Receptors in the Development of NAFLD." In Advances in Experimental Medicine and Biology, 45–53. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-8684-7_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Yona, Simon, Ki-Wook Kim, Rebecca Haffner, and Steffen Jung. "Unraveling Chemokine and Chemokine Receptor Expression Patterns Using Genetically Engineered Mice." In Methods in Molecular Biology, 129–44. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-426-5_8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Rodríguez-Frade, José Miguel, Laura Martinez Muñoz, Borja L. Holgado, and Mario Mellado. "Chemokine Receptor Dimerization and Chemotaxis." In Methods in Molecular Biology, 179–98. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-198-1_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Ford, Laura B., Chris A. H. Hansell, and Robert J. B. Nibbs. "Using Fluorescent Chemokine Uptake to Detect Chemokine Receptors by Fluorescent Activated Cell Sorting." In Methods in Molecular Biology, 203–14. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-426-5_13.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Wu, Yuntao. "Chemokine Receptor Signaling and HIV Infection." In Methods in Molecular Biology, 309–19. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-198-1_21.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Li, Meizhang. "Chemokine Receptors and Neural Stem Cells." In Methods in Molecular Biology, 49–55. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-426-5_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Chemokine biology"

1

"The Expression of Chemokine Genes in Neutrophiles Exposed to Leishmania." In International Conference on Cellular & Molecular Biology and Medical Sciences. Universal Researchers (UAE), 2016. http://dx.doi.org/10.17758/uruae.ae0916432.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Pienta, Kenneth J. "Abstract PL06-04: Targeting the tumor ecosystem: Translating the molecular biology of chemokine interactions to the clinic." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Nov 12-16, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1535-7163.targ-11-pl06-04.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Fang, Wei Bin, Nabil Alhakamy, Cory Berkland, and Nikki Cheng. "Abstract A063: Targeting the CCL2 chemokine pathway in breast tumors through intratumoral delivery of calcium cross linked TAT peptide: siRNA complexes." In Abstracts: AACR Special Conference on Advances in Breast Cancer Research: Genetics, Biology, and Clinical Applications - October 3-6, 2013; San Diego, CA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1557-3125.advbc-a063.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Taylor, Sheryse, Julian Candia, Adriana Zingone, John Tsang, and Brid Ryan. "Abstract PO-234: Relationship between increased concentrations of circulating chemokines and population differences in tumor biology." In Abstracts: AACR Virtual Conference: Thirteenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; October 2-4, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7755.disp20-po-234.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Sikorska, D., R. Rutkowski, J. Łuczak, W. Samborski, and J. Witowski. "AB0206 INTERLEUKIN-17 and CC-CHEMOKINE ligand 20 are not useful markers of rheumatoid arthritis activity in patients undergoing biologic treatment." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.2178.

Full text
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Chemokine biology' for particular source types:
Journal articles Dissertations / Theses Books
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography