scholarly journals A Polymorphism in C-C Chemokine Receptor 5 (CCR5) Associates with Löfgren’s Syndrome and Alters Receptor Expression as well as Functional Response

Cells ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1967
Author(s):  
Bekir Karakaya ◽  
Coline H. M. van Moorsel ◽  
Marcel Veltkamp ◽  
Claudia Roodenburg-Benschop ◽  
Karin M. Kazemier ◽  
...  
Keyword(s):  
Chemokine Receptor ◽  
Calcium Influx ◽  
Receptor Expression ◽  
Ccr5 Expression ◽  
Ccr5 Gene ◽  
Single Nucleotide ◽  
Inflammatory Protein ◽  
Löfgren’S Syndrome ◽  
And Function ◽  
Chemokine Receptor 5

C-C chemokine receptor 5 (CCR5) and polymorphisms in CCR5 gene are associated with sarcoidosis and Löfgren’s syndrome. Löfgren’s syndrome is an acute and usually self-remitting phenotype of sarcoidosis. We investigated whether the single nucleotide polymorphism (SNP) rs1799987 is associated with susceptibility for Löfgren’s syndrome and has an effect on CCR5 expression on monocytes and function of CCR5. A total of 106 patients with Löfgren’s syndrome and 257 controls were genotyped for rs1799987. Expression of CCR5 on monocytes was measured by flowcytometry. We evaluated calcium influx kinetics following stimulation upon N-formylmethionyl-leucyl-phenylalanine (fMLP) and macrophage inflammatory protein-1α (MIP-1α) on monocytes by measuring the median fluorescence intensity (MFI). The frequency of the G allele of rs1799987 was significantly higher in Löfgren’s syndrome than in healthy controls (p = 0.0015, confidence interval (CI) 1.22–2.32, odds ratio (OR) 1.680). Patients with a GG genotype showed higher CCR5 expression on monocytes than patients with the AA genotype (p = 0.026). A significantly (p = 0.027) lower count of patients with the GG genotype showed a calcium influx reaction to simulation upon MIP-1 α, compared with patients with the AA genotype. The rs1799987 G allele in CCR5 gene is associated with susceptibility to Löfgren’s syndrome and with quantitative and qualitative changes in CCR5, potentially effecting the inflammatory response.

scholarly journals Airway smooth muscle chemokine receptor expression and function in asthma

2009 ◽  
Vol 39 (11) ◽  
pp. 1684-1692 ◽  
Author(s):  
R. Saunders ◽  
A. Sutcliffe ◽  
D. Kaur ◽  
S. Siddiqui ◽  
F. Hollins ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Chemokine Receptor ◽  
Receptor Expression ◽  
Chemokine Receptor Expression ◽  
And Function

Regulation of CCR6 chemokine receptor expression and responsiveness to macrophage inflammatory protein-3α/CCL20 in human B cells

Blood ◽  
2000 ◽  
Vol 96 (7) ◽  
pp. 2338-2345 ◽  
Author(s):  
Roman Krzysiek ◽  
Eric A. Lefevre ◽  
Jérôme Bernard ◽  
Arnaud Foussat ◽  
Pierre Galanaud ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
B Cells ◽  
B Cell ◽  
Chemokine Receptor ◽  
Memory B Cells ◽  
Receptor Expression ◽  
B Cell Differentiation ◽  
Hematopoietic Stem ◽  
Inflammatory Protein ◽  
Macrophage Inflammatory Protein

Abstract The regulation of CCR6 (chemokine receptor 6) expression during B-cell ontogeny and antigen-driven B-cell differentiation was analyzed. None of the CD34+Lin− hematopoietic stem cell progenitors or the CD34+CD19+ (pro-B) or the CD19+CD10+ (pre-B/immature B cells) B-cell progenitors expressed CCR6. CCR6 is acquired when CD10 is lost and B-cell progeny matures, entering into the surface immunoglobulin D+ (sIgD+) mature B-cell pool. CCR6 is expressed by all bone marrow–, umbilical cord blood–, and peripheral blood–derived naive and/or memory B cells but is absent from germinal center (GC) B cells of secondary lymphoid organs. CCR6 is down-regulated after B-cell antigen receptor triggering and remains absent during differentiation into immunoglobulin-secreting plasma cells, whereas it is reacquired at the stage of post-GC memory B cells. Thus, within the B-cell compartment, CCR6 expression is restricted to functionally mature cells capable of responding to antigen challenge. In transmigration chemotactic assays, macrophage inflammatory protein (MIP)-3α/CC chemokine ligand 20 (CCL20) induced vigorous migration of B cells with differential chemotactic preference toward sIgD− memory B cells. These data suggest that restricted patterns of CCR6 expression and MIP-3α/CCL20 responsiveness are integral parts of the process of B-lineage maturation and antigen-driven B-cell differentiation.

Soluble HLA-G dampens CD94/NKG2A expression and function and differentially modulates chemotaxis and cytokine and chemokine secretion in CD56bright and CD56dim NK cells

Blood ◽  
2011 ◽  
Vol 118 (22) ◽  
pp. 5840-5850 ◽  
Author(s):  
Fabio Morandi ◽  
Elisa Ferretti ◽  
Roberta Castriconi ◽  
Alessandra Dondero ◽  
Andrea Petretto ◽  
...  
Keyword(s):  
Nk Cells ◽  
Chemokine Receptor ◽  
Nk Cell ◽  
Receptor Expression ◽  
Regulated Secretion ◽  
Cell Functions ◽  
Soluble Hla ◽  
Ifn Γ ◽  
And Function ◽  
Nk Receptor

Abstract Soluble HLA-G (sHLA-G) inhibits natural killer (NK) cell functions. Here, we investigated sHLA-G–mediated modulation of (1) chemokine receptor and NK receptor expression and function and (2) cytokine and chemokine secretion in CD56bright and CD56dim NK cells. sHLA-G-treated or untreated peripheral blood (PB) and tonsil NK cells were analyzed for chemokine receptor and NK receptor expression by flow cytometry. sHLA-G down-modulated (1) CXCR3 on PB and tonsil CD56bright and CD56dim, (2) CCR2 on PB and tonsil CD56bright, (3) CX3CR1 on PB CD56dim, (4) CXCR5 on tonsil CD56dim, and (5) CD94/NKG2A on PB and tonsil CD56bright and CD56dim NK cells. Such sHLA-G–mediated down-modulations were reverted by adding anti–HLA-G or anti–ILT2 mAbs. sHLA-G inhibited chemotaxis of (1) PB NK cells toward CXCL10, CXCL11, and CX3CL1 and (2) PB CD56bright NK cells toward CCL2 and CXCL10. IFN-γ secretion induced by NKp46 engagement was inhibited by NKG2A engagement in untreated but not in sHLA-G–treated NK cells. sHLA-G up-regulated secretion of (1) CCL22 in CD56bright and CD56dim and (2) CCL2, CCL8, and CXCL2-CXCL3 in CD56dim PB NK cells. Signal transduction experiments showed sHLA-G–mediated down-modulation of Stat5 phosphorylation in PB NK cells. In conclusion, our data delineated novel mechanisms of sHLA-G–mediated inhibition of NK-cell functions.

CCR5 expression on macrophages/microglia is associated with early remyelination in multiple sclerosis lesions

2008 ◽  
Vol 14 (6) ◽  
pp. 728-733 ◽  
Author(s):  
C Trebst ◽  
F König ◽  
RM Ransohoff ◽  
W Brück ◽  
M Stangel
Keyword(s):  
Multiple Sclerosis ◽  
Chemokine Receptor ◽  
Expression Profiles ◽  
Receptor Expression ◽  
Disease Course ◽  
Ccr5 Expression ◽  
Early Disease ◽  
Biopsy Material ◽  
Underlying Mechanisms

Remyelination in multiple sclerosis (MS) occurs spontaneously and extensively. The underlying mechanisms, however, are only partly understood. Findings in experimental animal settings suggest that inflammation promotes remyelination and repair. Here, we characterized the chemokine receptor expression profiles of macrophages/microglia in early remyelinating and completely remyelinated lesions compared with active demyelinating and inactive demyelinated MS lesions obtained in the early disease course. Biopsy material consisting of 16 MS cases was available for this study. We found that macrophages/microglia within early remyelinating lesions expressed predominantly CCR5. Our findings implicate a possible role of CCR5+ cells in initiating remyelination.

scholarly journals Cysteine-cysteine chemokine receptor 5 (CCR5) profile of HIV-infected subjects attending University of Calabar Teaching Hospital, Calabar, Southern Nigeria

2019 ◽  
Author(s):  
Ekerette Friday Ekere ◽  
Monday F. Useh ◽  
Henshaw Uchechi Okoroiwu ◽  
Tatfeng Youtchou Mirabeau
Keyword(s):  
Teaching Hospital ◽  
Chemokine Receptor ◽  
Critical Role ◽  
Rapid Progression ◽  
Ccr5 Gene ◽  
Mutant Type ◽  
Base Pair Deletion ◽  
Polymerase Chain ◽  
Type Gene ◽  
Chemokine Receptor 5

Abstract Background Cysteine-cysteine chemokine receptor 5 is the main HIV co-receptor involved in the virus and cell-to-cell spread. A variant of the CCR5 gene known as CCR5-Δ32 which is a product of 32 base pair deletion in the gene plays critical role in the infection and progression to AIDS. The study was done to determine the CCR5 genotype of HIV-infected subjects attending University of Calabar Teaching Hospital, Calabar. Methods A total of 100 subjects attending HIV clinic, University of Calabar Teaching Hospital were purposively recruited for this study. DNA was extracted from each sample using the quick gDNA miniprep DNA extraction kit. Polymerase chain reaction was used in amplification of CCR5 gene in each DNA in a 9700 ABI Thermo cycler and then resolved on 4% agarose gel electrophoresis. Result Out of the 100 samples assessed, 100 (100%) were homozygous for the CCR5 wild type gene (CCR5-wt), while none (0%) was homozygous for the CCR5-Δ32 (mutant type), and heterozygosity was not observed. Conclusion This study observed absence of CCR5-Δ32 deletion gene among the studied subjects in Calabar. This implies lack of genetic advantage in HIV infection and possible rapid progression towards AIDS if other precautions are not checked.

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