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1

New biodefense strategies by neutrophils

100%
Ishikawa F., Miyazaki S.
Archivum Immunologiae et Therapiae Experimentalis
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2005
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vol. 53
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issue 3
226-233
EN
Chemokines and other chemotactic factors induce neutrophils, macrophages, and dendritic cells to migrate to an inflammatory site and efficiently ingest and destroy infective microorganisms. Moreover, antigen-presenting cells, such as macrophages and dendritic cells, present the microbial antigens via major histocompatibility complex class II molecules, resulting in the activation of specific CD4 T cells. Since neutrophils have a short life-span and are highly susceptible to apoptosis, their role in antigen presentation has been questioned. However, various pro-inflammatory cytokines, such as interleukin (IL)-1, IL-6, tumor necrosis factor a, and interferon g, produced at the site of inflammation activate neutrophils and suppress apoptotic death. These cytokine-activated neutrophils show enhanced expression of cell surface molecules and become as competent as dendritic cells and macrophages in their ability of antigen presentation. Traditionally, neutrophils are known to be responsible for innate immunity, and recently they are also considered to be intimately associated with the establishment of acquired immunity. In the present review on the role of neutrophils we describe both classic innate and acquired immunity.
2

Serum concentrations of MCP-1 and RANTES in patients during aortic surgery: the relationship with ischemia-reperfusion

100%
Jedynak M., Siemiatkowski A., Gacko M., Mroczko B., Borkowski J.
Archivum Immunologiae et Therapiae Experimentalis
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2004
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vol. 52
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issue 3
201-207
EN
Surgical trauma is associated with depression of the immune system, which results in a high complication rate following abdominal aortic aneurysm (AAA) repair. Monocyte chemotactic protein-1 (MCP-1) and regulated-on-activation normal T cell expressed and secreted (RANTES) protein are important mediators of the immune and inflammatory response. The aim of this study was to determine whether there is any relationship between MCP-1 or RANTES and operative injury and ischemia-reperfusion during AAA surgery in human. Peripheral blood samples were taken from 12 patients before surgery, after anesthesia induction, before unclamping of aorta (PreXoff), 90 min after unclamping (90minXoff), and at 24 and 48 h after surgery. The MCP-1 and RANTES serum concentrations were measured with the ELISA technique. MCP-1 concentration significantly increased after reperfusion (90minXoff) in comparison with the PreXoff level (p=0.001). Twenty-four hours after AAA repair, MCP-1 significantly decreased 269?225 pg/ml (p=0.005) and reached preoperative value. RANTES level was higher in AAA patients before surgery than in controls (p=0.025) and decreased significantly after ischemia-reperfusion to 13 ng/ml (p< 0.001) at 90minXoff. We showed increases in RANTES concentration to 26 ng/ml on the 1st and to 31 ng/ml on the 2nd day after surgery (p=0.020, p=0.012, respectively) compared with the 90minXoff level. Ischemia-reperfusion during AAA repair results in an increase in MCP-1 and decrease in RANTES concentrations in serum. The changes in chemokine concentrations may influence the development of immunosuppression after AAA repair, contributing to the postoperative course.
3

A burgeoning family of biological mediators: chemokines and chemokine receptors

100%
Le Y., Gong W., Shen W., Li B., Dunlop N. M., Wang J. M.
|
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vol. 48
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issue 3
143-150
EN
Chemokines are a superfamily of pro-inflammatory polypeptide cytokines that selectively attract and activate different cell types. Most of its members are small proteins that exhibit conserved cysteines in specific positions. Chemokines activate cells through their binding to shared or unique cell surface receptors which belong to the seven-transmembrane (STM), G-protein-coupled receptors (GPCRs). The large number of chemokines and chemokine receptors are indicative of the importance of these molecules in a variety of pathophysiological conditions.
4

Targeting the chemokine network in renal inflammation

100%
Eis V., Vielhauer V., Anders H.-J.
Archivum Immunologiae et Therapiae Experimentalis
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2004
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vol. 52
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issue 3
164-172
EN
Chemokines and their receptors are involved in the pathogenesis of renal diseases. They mediate leukocyte recruitment and activation during initiation as well as progression of renal inflammation. Infiltrating leukocyte subpopulations contribute to renal damage by releasing inflammatory and profibrotic cytokines. All intrinsic renal cells are capable of chemokine secretion on stimulation in vitro. Expression of inflammatory chemokines correlates with renal damage and local accumulation of chemokine receptor-bearing leukocytes in a variety of animal models of renal diseases as well as in human biopsy studies. Chemokines and their respective receptors could represent new targets for therapeutic intervention in renal inflammatory disease states that often tend to progress to end-stage renal disease. This article summarizes the present data on the role of chemokines and their receptors in renal inflammation with special emphasis on our efforts to identify the chemokine receptors CCR1 and CCR2 as promising targets for therapeutic intervention.
5

All roads lead to Rome: pathways of NKT cells promoting asthma

100%
Jinquan T., Li W., Yuling H., Lang C.
Archivum Immunologiae et Therapiae Experimentalis
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2006
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vol. 54
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issue 5
335-340
EN
NKT cells are the prominent manipulator in asthma development. Asthmatic NKT cells migrate from thymus, spleen, liver and bone marrow into blood vessels, and then concentrate in airway bronchi mucosa. This recruitment is dependent on high expression of CCR9 and engagement of CCL25/CCR9. NKT cells promote asthma in two different pathways. One is an indirect pathway. NKT cells contact with CD3+ T cells and induce them secreting large quantity of Th2 cytokines (IL-4, IL-13), which requires the participation of dentritic cells and the synergic signaling of CCL25/CCR9 and CD226. The other is a direct pathway. Circulating asthmatic NKT cells selectively highly express Th1 cytokines . Once reached airway epithelium, most NKT cells shift to Th2-bias, highly expressing IL-4, IL-13, but not IFN-alpha. Both pathways lead to airway hyperresponsiveness and inflammation, asthma development. Comparing to the well documented suppressive regulatory T cells, CD4+CD25+ T cells, NKT cells perform as a novel active regulator in asthma. These recent understanding of NKT cells performance in the development of asthma might unveil new therapy targets and management strategies for asthma.
6

Chemokines, G proteins and natural killer cells

88%
Maghazachi A. A.
|
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vol. 48
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issue 2
65-72
EN
Natural killer (NK) cells are anti-tumor and anti-viral effector cells. Members of C, CC, CXC and CX3C chemokines induce the chemotaxis and enhance the cytotoxicity of NK cells, suggesting that these cells express receptors for chemokines. The ability of members of chemokines to inhibit the replication of HIV-1 strains, combined with the ability of the same chemokines to activate the anti-viral NK cells, provide compelling evidence for the role of NK cells in eradicating HIV-1 infection. In addition, chemokines induce various intracellular signaling pathways in NK cells, which include activation of the heterotrimeric, and perhaps the small guanine nucleotide binding (G) proteins, as well as the mobilization of intracellular calcium, among other activities. Further, chemokines induce the phosphorylation of chemokine receptors through the recruitment of G protein-coupled receptor kinases (GRKs) resulting in the desensitization and turning off the signals. In this review, I will update the knowledge of the effect of chemokines on NK cell motility and the signal transduction pathways induced by chemokines in these cells.
7

Factors underlying chronic inflammation in rheumatoid arthritis

88%
Wong S. H., Lord J. M.
Archivum Immunologiae et Therapiae Experimentalis
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2004
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vol. 52
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issue 6
379-388
EN
Rheumatoid arthritis (RA) is a debilitating chronic inflammatory disease whose characteristic pathology includes swollen, painful, and deformed joints. In recent decades, both clinical and basic scientific research have tried to determine the factors involved in the pathogenesis of this common disease. Although the cause of RA is still unknown, several factors that contribute to RA have been identified. Among these are the discoveries of: susceptibility genes, disease-causing immune cells, and cytokine and signal transduction networks involved in promoting persistence of inflammation. Various therapeutic strategies, including anti-tumor necrosis factor alpha therapy, have been developed to target one or more of these factors. Although none of these therapeutic strategies can actually cure the disease, some of these novel agents have proven to be more effective than others. This implies that the success of a therapy is very much dependent on the therapeutic targets chosen. Therefore, improved understanding of the cellular and molecular events occurring in the rheumatoid joint during the pathogenesis of the disease is particularly important if we are to better combined therapeutic strategies. In this article we summarize current understanding of the factors that contribute to disease pathogenesis in RA and identify cellular and molecular events that could drive the development of the disease and represent potential new therapeutic targets.
8

Sequence variants of chemokine receptor genes and susceptibility to HIV-1 infection

88%
Parczewski M., Leszczyszyn-Pynka M., Kaczmarczyk M., Adler G., Binczak-Kuleta A., Loniewska B., Boron-Kaczmarska A., Ciechanowicz A.
Journal of Applied Genetics
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2009
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vol. 50
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issue 2
159-165
EN
Genetic susceptibility to HIV infection was previously proven to be influenced by some chemokine receptor polymorphisms clustering on chromosome 3p21. Here the influence of 5 genetic variants was studied: D32 CCR5, G(?2459)A CCR5, G190A CCR2, G744A CX3CR1 and C838T CX3CR1. They were screened in a cohort of 168 HIV-1 positive adults [HIV(+) group] and 151 newborns [control group] from northwestern Poland. PCR-RFLP was performed to screen for the variants (except for D32 CCR5 polymorphism, where PCR fragment size was sufficient to identify the alleles) and then electrophoresed on agarose gel to determine fragment size. Distribution of genotypes and alleles was not significantly different between the groups except for the CCR5 polymorphisms, with the D32 allele and the (?2459)A CCR5 allele more frequent among neonates than in the HIV(+) group. No D32/D32 homozygotes were found in the HIV(+) group, but 16.1% were D32/wt heterozygotes. In the control group, 1.3% were D32/D32 homozygotes and 26.0% were D32/wt heterozygotes. Linkage between the chemokine polymorphisms was calculated using the most informative loci for haplotype reconstruction. Haplotypes containing D32 CCR5, 190G CCR2 and 744A CX3CR1 were found to be significantly more common in the control group. This suggests an association between these haplotypes and resistance to HIV-1 infection.
9

T cell integrin activation by chemokines in inflammation

88%
Tanaka Y.
|
EN
The adhesive function of integrins is regulated through cytoplasmic signaling induced by several stimuli, whose process is designated ?inside-out signaling?. A large number of lymphocytes are recruited to the sites of inflammation where they form an essential component of the response to infection, injury, autoimmune disorders, allergy, tumor invasion, atherosclerosis and so on. The recruitment of leukocytes into tissue is regulated by a sequences of interactions between the circulating leukocytes and the endothelial cells. Leukocyte integrins play a pivotal role in leukocyte adhesion to endothelial cells. During the process, the activation of integrins by chemokines, is essential for integrin-mediated adhesion in which a signal transduced to the leukocyte converts the functionally inactive integrin to an active adhesive configuration. The present review documents the relevance of cytoplasmic signaling and cytoskeletal assembly to integrin-mediated adhesion induced by chemokines during inflammatory processes.
10

How endothelial cell organo-specificity mediates circulating cell homing

88%
Kieda C.
Archivum Immunologiae et Therapiae Experimentalis
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2003
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vol. 51
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issue 2
81-89
EN
Normal and transformed cells are homing from the circulation into tissues in a very selective way thanks to highly complex molecular mechanisms that govern cell-to-cell interactions and drive the homing of circulating cells to be achieved properly. Because this is characterised by a resulting high selectivity, it constitutes a template for targeted drug-, gene- or cell-therapy strategies. Designing a mimetic-based therapy requires the identification of the responsible selective molecules but also, their mechanisms of action and interactions with their ligands, together with their biological modulation and regulation. This homing/invasion event happens to be decisive at the level of the endothelium that lines the vessel walls. Since cell-to-cell interactions mean a double recognition process, this review will illustrate the part played by the endothelial cells (EC) and their adhesion molecules: the protein as well as the glycan part point of view, the chronology and environmental modulation of EC adhesion molecules expression. These characteristics should provide keys to understand the resulting overall specificity of cell localisation. Taking into account the cytokine microenvironment, it was recently documented a fundamental role for locally secreted chemokines which act through their restricted presentation by endothelial cells. As such, chemokines contribute to illustrate the concept of endothelial organo-specificity which is approached here uncovering the role of glycoconjugates signalling as the hallmark of refined cellular recognitions and discussed, in the context of potential drug design against site-directed diseases as metastases, inflammatory leukocytes recruitment, tumour/inflammation-induced angiogenesis.
11

The inflammatory response in M. tuberculosis infection

75%
Toossi Z.
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vol. 48
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issue 5
513-520
EN
Infection with Mycobacterium tuberculosis (MTB) is accompanied by an intense local inflammatory response which may be critical to the pathogenesis of tuberculosis. Activation of components of the innate immune response, such as recruitment of polymorphonuclear (PMN) and mononuclear phagocytes and induction of pro-inflammatory cytokines, such as tumor necrosis factor alpha (TNF-alpha), by MTB occurs early after MTB infection, however, may persist as the organism establishes itself within granulomas. MTB and its protein and non-protein components are potent in induction of cytokines and chemokines from PMN and monocytes. This review focuses on the interaction of MTB and the host with regard to activation of the innate immune response. It also attempts to identify the potential impact of this early response on the subsequent pathogenesis of MTB, and its role in development and extent of tuberculosis. Insights into the initiation and persistent of the inflammatory response may allow the application of anti-inflammatory agents as adjuncts in the treatment of tuberculosis.
12

Mast cells and cytokines - new insight into the participation of mast cells in inflamatory reactions

75%
Kuprys I., Kuna P.
Postępy Higieny i Medycyny Doświadczalnej
|
1996
|
vol. 50
|
issue 1
43-63
EN
Tissue mast cells are multifunctional immune cells and have been implicated in allergic and inflammatory reactions. They used to be regarded merely as a source of histamin, prostaglandins and leukotriens which mediated the symptoms of the acute allergic reaction but more recent work has indicated they are involved in many inflammatory reactions. The discavory of production and secretion of a unique array of cytokines by these cells has suggested new ways in which they could influence to the development of inflammation. Many experiments have disclosed that mast cells owning to cytokines can not only initiate but also regulate and modulate this process. With the results come the realisation that these cytokines might represent important effector molecules in a variety of pathologic and physiologic processes where mast cells involvment had been postulated but an understanding of the mechanisms remained obscure. The aim of this article is introduction the biology of mast cells and presentation the information concern production and secretion of cytokines by these cells like also influence of these biologically active molecules on inflammatory process.
13

T cell chemokine receptor expression in human Th1- and Th2-associated diseases

75%
Campbell J. D., Hayglass K. T.
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vol. 48
|
issue 5
451-456
EN
The interaction between chemokines and their receptors is an important step in the control of leukocyte migration into sites of inflammation. Chemokines also mediate a variety of effects independent of chemotaxis, including induction and enhancement of Th1- and Th2---associated cytokine responses. Recent studies have shown that human Th1 and Th2 clones, activated under polarizing conditions with polyclonal stimuli in vitro, display distinct patterns of chemokine receptor expression: Th1 clones preferentially express CCR5 and CXCR3 while many Th2 clones express CCR4, CCR8 and, to a lesser extent, CCR3. These differential patterns of chemokine receptor expression suggest a mechanism for selective induction of migration and activation of Th1- and Th2-type cells during inflammation and, perhaps, normal immune homoeostasis. Studies have begun to examine T cell chemokine receptor expression in vivo to determine the relevance of these in vitro observations to human Th1 and Th2-associated diseases. In this review, we critically examine recent reports of T cell chemokine receptor expression in human autoimmune disorders (multiple sclerosis and rheumatoid arthritis) and atopic disorders (allergic rhinitis and asthma) which are believed to arise from inappropriate Th1- and Th2-dominated responses, respectively.
14

Association of CD45dimVLA-4+ cells with the NKT cell lineage and their selective expression of IL-13, IP-15, and CCR3 transcripts

75%
Matejuk A., Afentoulis M.
Archivum Immunologiae et Therapiae Experimentalis
|
2006
|
vol. 54
|
issue 3
183-191
EN
Estrogen (E2) was shown to prevent experimental autoimmune encephalomyelitis (EAE) and to produce a novel population of regulatory CD45dimVLA-4+ cells. Although their appearance was dependent upon an elevated hormonal level, E2 was not required for their production, as they also were induced by immunization with Mycobacterium tuberculosis as a component of complete Freund's adjuvant. Materials and Methods: Molecular techniques, including ribonuclease protection assays and quantitative RT-PCR, were used to provide further characterization of CD45dimVLA-4+ cells. Moreover, we determined the developmental requirements of the CD45dimVLA-4+ cells using genetically modified mice and extensive flow cytometry analysis. Results: Characterization of CD45dimVLA-4+ mRNA profile revealed highly elevated levels of CD16, CD44, CCR3, IP-15, and IL-13 transcripts compared with their CD45highVLA-4+ counterparts. Furthermore, we found up-regulation of anti-apoptotic bcl-w and bcl-xl genes and transcripts encoding the TCR and CD8 homodimer. The production of CD45dimVLA-4+ cells was evident in nude mice and in MHC class II- and 2-microglobulin, but not in CD1-deficient mice, suggesting a crucial role for CD1 in their induction.
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