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Chemokine Receptor

Chemokine Receptors are a family of cell surface proteins that bind to chemokines, a class of small cytokines that regulate cell trafficking and migration.
These receptors play a crucial role in various physiological and pathological processes, including immune responses, inflammation, and cancer metastasis.
Chemokine Receptors are G protein-coupled receptors that activate signal transduction pathways upon ligand binding, leading to changes in cellular behavior.
Studying Chemokine Receptors is essential for understanding the mechanisms underlying immune system function and developing potential therapeutic interventions for a wide range of diseases.
The PubCompare.ai platform can help researchers optimize their Chemokine Receptor research by providing access to the best protocols from literature, preprints, and patents, while leveraging AI-driven comparisons to ensure reproducible and accurate results.
This streamlines the research process and enables more informed decisions.

Most cited protocols related to «Chemokine Receptor»

1
Generation and Characterization of CCR2-RFP and CX3CR1-GFP Mice
Cited 59 times
CCR2RFP mice were created as described [25] (link) (see Figure 1 and Text S1). Founder mice were crossed with Cre-deleter mice [43] (link) to remove the neo gene and backcrossed onto the C57Bl/6 line nine times. To generate homozygous Ccr2RFP/RFPCx3cr1GFP/GFP mice, we crossed Ccr2RFP/RFP with Cx3cr1GFP/GFP C57Bl/6 mice (a gift of D.R. Littman), and the progeny were backcrossed onto C57Bl/6. Mice that had undergone chromosome recombination between the CCR2 and CX3CR1 loci were selected by being positive for both RFP and GFP by flow cytometry of tail vein blood.
Unless stated otherwise, all mice were backcrossed seven to nine times on C57Bl/6 and were 2–6 months of age at sacrifice. Some mice were crossed with C57Bl/6 Apoe−/− mice. These mice were fed a Western diet (42% of calories from fat) (Harlan Teklad, TD88137) for 8 weeks, starting at 6–8 weeks of age. All other mice were fed standard chow. Mice were bred at the Gladstone Institutes and the Biological Resources Unit, Cleveland Clinic, Lerner Research Institute. Animal experiments were performed according to the protocols approved by the Institutional Animal Care and Use Committee at the Cleveland Clinic, UCSF, and UTSA following the National Institute of Health guidelines for animal care. Mice were genotyped by PCR using tail DNA, and chemokine receptor–specific primers (Invitrogen, Carlsbad,CA) (Table S1).
Saederup N., Cardona A.E., Croft K., Mizutani M., Cotleur A.C., Tsou C.L., Ransohoff R.M, & Charo I.F. (2010). Selective Chemokine Receptor Usage by Central Nervous System Myeloid Cells in CCR2-Red Fluorescent Protein Knock-In Mice. PLoS ONE, 5(10), e13693.
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Publication 2010
Animals ApoE protein, human Biopharmaceuticals BLOOD Chemokine Receptor Chromosomes Flow Cytometry Genes Homozygote Institutional Animal Care and Use Committees Mice, House Mice, Inbred C57BL Oligonucleotide Primers Recombination, Genetic Tail Veins
2
Generating Mouse OSCC Cell Lines from Primary Tumors
Cited 28 times
Primary DMBA induced mouse OSCC were generated as described (26 (link)). Single cell suspensions of individual primary oral cavity tumors were made with Collagenase IA (Sigma-Aldrich) and cultured in IMDM/F12 (2:1) with 5% FCS, penicillin/streptomycin, 1% amphotericin, 5 ng/mL EGF (Millipore), 400 ng/mL hydrocortisone, and 5 μg/mL insulin. Sequential differential trypsinization was then used to clear fibroblast contamination. MOC1, 7, 10, 22 and 23 were derived from primary tumors in C57BL/6 WT mice and MOC2 was derived from a chemokine receptor CXCR3deficient mouse on a pure C57BL/6 background (27 (link)) (of note, no major differences in the incidence of tumor formation were noted between the different genotypes). CXCR3 is not detectable on oral keratinocytes and does not contribute to MOC2 growth (Figure S3). Immunofluorescence staining for cytokeratin was performed to confirm an epithelial phenotype (Figure 1C and Figure S1C). PCI-13 was obtained from Dr. Theresa Whiteside, UPCI:SCC029B and UPCI:SCC068 were obtained from Dr. Suzanne Gollin, and all were used with minimal passaging. The UM-SCC-1 cell line (from Dr. Tom Carey) was genotyped in May, 2011 and concordance with published data was established (27 (link)).
Judd N.P., Winkler A.E., Murillo-Sauca O., Brotman J.J., Law J.H., Lewis JS J.r., Dunn G.P., Bui J.D., Sunwoo J.B, & Uppaluri R. (2011). ERK1/2 regulation of CD44 modulates oral cancer aggressiveness. Cancer Research, 72(1), 365-374.
Publication 2011
9,10-Dimethyl-1,2-benzanthracene Amphotericin Cell Lines Cells Chemokine Receptor Collagenase CXCR3 protein, human Cytokeratin Fibroblasts Hydrocortisone Immunofluorescence Insulin Keratinocyte Mice, Inbred C57BL Mouth Neoplasms Mus Neoplasms Penicillins Phenotype Streptomycin
3
Hybrid Agent-Based Modeling of Tuberculosis Granuloma
Cited 22 times
The model presented here is an extension of a previous ABM that captured cellular interactions leading to granuloma formation during infection with Mtb (38 (link)). The model is considered hybrid since we incorporated both discrete entities (cells) and continuous entities (chemokines, TNF and Mtb) that interact simultaneously. ABMs are developed based on four considerations: an environment, agents that reside there, the rules that describe the agents and their interactions, and the timescales on which events are defined.
The environment represents a 2 mm × 2 mm section of lung parenchyma as a 100 × 100 square 2-dimensional lattice with individual micro-compartments scaled to the approximate size of a single macrophage: 20 μm in diameter (39 (link)). Discrete agents move on the lattice and respond to their environment based on rules reflecting known biological activities. Bacteria and effector molecules can reside anywhere on the lattice and undergo diffusion when appropriate.
Caseation represents inflammation of, and damage to, the lung parenchyma from macrophage cell death. We note a change of terminology to “caseation” from “necrosis” in previous work (38 (link)), as strict necrosis within the granuloma is now believed to be caused by substantial neutrophil infiltration and death, while caseation is likely initiated by macrophage death (unpublished data, JLF). In the ABM, caseation is defined to occur when a threshold number of activated or infected macrophage deaths take place in a micro-compartment. A final environmental feature is designation of spaces as vascular sources.
We include two types of discrete agents in the model: macrophages and T cells. As previously (20 (link), 38 (link)), macrophage agents are either resting (Mr, uninfected), infected (Mi; have taken up bacteria), chronically infected (Mci; are unable to clear their intracellular bacterial load), or activated (Ma; can effectively kill bacteria). In contrast to our previous study (38 (link)), where a single T cell class captured all cell behaviors, here we represent three distinct T cell subpopulations based on function: the Tγ class captures CD4+ and CD8+ pro-inflammatory T cells; Tc represent cytotoxic T cells; and Treg represent regulatory T cells. In this representation, all T cells in a particular class have identical function; this is simpler than in vivo, but we capture enough detail in this representation for a qualitative representation of known T cell effects.
In addition to the discrete entities, extracellular bacteria, diffusing effector molecules (CCL2, CCL5, CXCL9/10/11 and TNF) are agents (concentrations) that are tracked continuously over time. The chemokine model used here is a simplification that was chosen to include a ligand for each key chemokine receptor, while minimizing the distinct chemokine classes represented to save on computation.
Cells respond to signals in the surrounding environment according to rules that represent known activities in vivo. During simulations, each agent responds depending on its state. Examples of rules include uptake of bacteria, macrophage activation by T cells, secretion of cytokines and chemokines, etc. For a full list of rules, see Supplement 1.
Ray J.C., Flynn J.L, & Kirschner D.E. (2009). Synergy between individual tumor necrosis factor-dependent functions determines granuloma performance for controlling Mycobacterium tuberculosis infection. Journal of immunology (Baltimore, Md. : 1950), 182(6), 3706-3717.
Publication 2009
As-A 2 Bacteria Biopharmaceuticals Blood Vessel CCL2 protein, human CCL5 protein, human CD8-Positive T-Lymphocytes Cell Communication Cells Chemokine Chemokine Receptor CXCL9 protein, human Cytokine Cytotoxic T-Lymphocytes Dietary Supplements Granuloma Hybrids Infection Inflammation Ligands Lung Macrophage Macrophage Activation Macrophages, Alveolar Necrosis Neutrophil Infiltration Population Group Protoplasm Regulatory T-Lymphocytes secretion T-Lymphocyte
4
Modeling Immune Cell Migration in Toxoplasma Infection
Cited 12 times
T. gondii infection was established by intraperitoneal injection of ovalbumin-expressing Prugnauid strain (PruOVA) tachyzoites. Real time PCR was performed for chemokine receptor expression and T. gondii DNA quantification. Brain mononuclear cells were stained with fluorescently conjugated antibodies for flow cytometric analysis. OT-I cells were activated in vitro and transferred to recipient mice. Mice were treated with four doses of 100 μg of anti-CXCL10 for week-long depletion studies or 300 μg 18 hours prior to imaging studies. Pertussis toxin was administered at 400 μg/kg six hours before imaging. For MP microscopy, explant brain was imaged using a Leica SP5 2-photon microscopy system. Cell tracking was performed using Volocity software. In order to create displacement histograms without binning artifacts30 (link) (Supplementary Tables 2-3), a constant number of displacements were placed in each bin. Various statistical methods were applied to test the validity of the generalized Lévy walk model (see Fig. 3, Supplementary Figs. 3, 5, 7, 8, 10, Supplementary Table 1, and Supplementary Discussion). Brownian dynamics-like simulations were performed to simulate the general behavior and searching capability of Gaussian (“random”) and Lévy walkers (see Supplementary Discussion). N searchers were placed in a spherical volume of radius b, and they moved stochastically until finding the target of radius a, which was stationary at the center of the sphere. During random walks, searchers moved 6DΔt = 0.1μm in the x-, y-, or z-direction each time step; here D is the motility coefficient and Δt is the time step. In Lévy walk simulations, a direction for a run was chosen at random, and run lengths were drawn from a Lévy distribution with exponent μrun=2.15. Searchers moved a distance vΔt each time step until the run was completed. After each run, the walker paused for a time drawn from Lévy distribution with μpause=1.7.
Harris T.H., Banigan E.J., Christian D.A., Konradt C., Wojno E.D., Norose K., Wilson E.H., John B., Weninger W., Luster A.D., Liu A.J, & Hunter C.A. (2012). Generalized Lévy walks and the role of chemokines in migration of effector CD8+ T cells. Nature, 486(7404), 545-548.
Publication 2012
Antibodies Brain Cells Chemokine Receptor Displacement, Psychology Figs Flow Cytometry Infection Injections, Intraperitoneal Microscopy Motility, Cell Mus Ovalbumin Pertussis Toxin Radius Real-Time Polymerase Chain Reaction Strains T-DNA Walkers
5
Flow Cytometry Analysis of T Cell Subsets
Cited 9 times
T cells were stained with the relevant antibody on ice for 30 min (chemokine receptor staining performed at room temperature for 20 min) in PBS buffer containing 2% FCS and 0.1% sodium azide. Cells were then washed twice, fixed with 1% paraformaldehyde, and analyzed with a FACSCalibur or FACSAria flow cytometer. Live cells were gated based on forward and side scatter properties, and analysis was performed using FlowJo software (Tree Star, http://www.treestar.com). The following anti-human antibodies were used for staining: CD3, CD4, CD8, CD45RO, CD45RA, CD28, CD27, CD11b, CD57, CD7, CD62L, HLA-DR, CCR5 (all from BD Biosciences), CCR7, and CCR4 (R&D Systems). The CRTH2 antibody used for these experiments has been previously described [41 (link)]. Secondary goat-anti-mouse antibodies were conjugated with allophycocyanin or PE (BD Biosciences). For the intracellular p24 stain, fixation and permeabilization was performed using a commercial kit (BD Biosciences) according to the manufacturer's instructions. Subsequently, cells were stained with anti-p24 for 1 h, followed by goat-anti-mouse conjugated to allophycocyanin for 30 min.
Oswald-Richter K., Grill S.M., Leelawong M., Tseng M., Kalams S.A., Hulgan T., Haas D.W, & Unutmaz D. (2007). Identification of a CCR5-Expressing T Cell Subset That Is Resistant to R5-Tropic HIV Infection. PLoS Pathogens, 3(4), e58.
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Publication 2007
allophycocyanin Anti-Antibodies Buffers CCR5 protein, human CD45RO Antigens Cells Chemokine Receptor Goat HLA-DR Antigens Homo sapiens Immunoglobulins ITGAM protein, human Mus paraform Protoplasm SELL protein, human Sodium Azide T-Lymphocyte Trees

Most recents protocols related to «Chemokine Receptor»

1
Engineered Tregs for Autoimmune Therapy
Not available on PMC !

Example 2

CD4+/CD45RA+ T-cells are transduced with a lentivirus having nucleic acid sequences encoding a FOXP3 polypeptide having mutations as described herein, a receptor polypeptide, and a therapeutic gene product (FIG. 2). Here, a CD4+/CD45RA+ T-cell is transformed with a nucleic acid sequence encoding a FOXP3 polypeptide, a nucleic acid sequence encoding a CXCR3 chemokine receptor polypeptide, and is also transformed with a nucleic acid sequence encoding a scFv antigen-binding fragment that is capable of binding to an IL-6R antigen expressed on a cell associated with an autoimmune disease. The binding of the scFV to an epitope of IL-6R blocks the binding of IL-6R to IL-6. An antibody used in this example includes Tocilizumab, which is a humanized anti-IL-6R antibody. The variable light and heavy chain domains of Tocilizumab (See, U.S. Pat. No. 5,795,965) are provided to the cells using nucleic acid sequence encoding a scFv linked to a secretion signal and operably linked by a constitutive promoter such as EF-1α. Mutations are introduced into the amino acid sequence of Tocilizumab that render the heavy and light chains more favorable binding properties to the IL-6R (See, U.S. Pat. No. 8,562,991). Tregs are not known to naturally produce IL-6 blocking mediators (e.g., antibody or antigen-binding fragments to IL-6R). Therefore, expression of such blockers transformed into a CD4+/CD45RA+ T-cell along with an a nucleic acid sequence encoding a FOXP3 polypeptide will render the T-cells more effective in inflammatory environments than T-cells not transformed with the nucleic acid sequences described herein. The binding of the scFv to IL-6R+ is confirmed by flow cytometry. Secretion of the scFv is verified by ELISA, and the biological activity is confirmed by inhibition of IL-6 signaling in a reporter cell assay (e.g., IL-6 Luciferase stable reporter cell line from Novus Biologicals).

US11879003B2. Methods for increasing T-cell function (2024-01-23). Kyverna Therapeutics, Inc. [US]. Inventors: John Lee [US], Erin O'Brien [US], Jordan Tsai [US], Lih-Yun Hsu [US], Faye Wu [US].
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Patent 2024
Amino Acid Sequence Antibodies, Anti-Idiotypic Antigens Autoimmune Diseases Base Sequence Biological Assay Biological Factors Biopharmaceuticals CD4 Positive T Lymphocytes Cell Lines Cells Chemokine Chemokine Receptor CXCR3 protein, human CXCR3 Receptors Enzyme-Linked Immunosorbent Assay Epitopes Flow Cytometry IL6R protein, human Immunoglobulins Immunoglobulins, Fab Inflammation Lentivirus Light Luciferases Mutation Novus Polypeptides Proteins Psychological Inhibition secretion T-Lymphocyte Therapeutics tocilizumab
2
Generating CXCR3+ Regulatory T-cells
Not available on PMC !

Example 3

CD4+CD45RA+ T-cells are transduced with a lentivirus having nucleic acid sequences encoding a CXCR3 polypeptide and a nucleic acid sequence encoding a FOXP3 polypeptide (FIG. 3). Following transformation, the cells are expanded in the presence of high dose rIL-2 and purified based on low expression of CD127 (IL7 receptor). Other means of purifying the cells as described herein or known in the art can also be used to purify the T-cell. CXCR3 expression is confirmed by flow cytometric analysis using an antibody against the CXCR3 polypeptide (e.g., anti-human CD183 (CXCR3) Biolegend Cat. No. RU0353707). CXCR3 function is also confirmed by an in vitro chemotaxis assay (e.g., transwell migration assay). Briefly, transduced cells are placed in a transwell system with a CXCR3 ligand (e.g., 50-300 ng/mL CXCL10 (human rCXCL10 from R&D Systems Cat No. 266-IP-010)) or a control chemokine present on the side of the membrane opposite the transduced cells. Migration of cells across the membrane is evaluated by flow cytometry using an antibody against CXCR3. Specificity is further confirmed by blocking migration with anti-CXCR3 blocking antibody.

US11879003B2. Methods for increasing T-cell function (2024-01-23). Kyverna Therapeutics, Inc. [US]. Inventors: John Lee [US], Erin O'Brien [US], Jordan Tsai [US], Lih-Yun Hsu [US], Faye Wu [US].
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Patent 2024
Antibodies, Anti-Idiotypic Base Sequence Biological Assay Cardiac Arrest Cell Migration Assays Cells Chemokine Chemokine Receptor Chemotaxis CXCR3 protein, human Flow Cytometry Homo sapiens Immunoglobulins Interleukin 7 Receptor Lentivirus Ligands Migration, Cell Polypeptides T-Lymphocyte Tissue, Membrane Tissues
3
Quantitative Analysis of Immune Cell Phenotypes
For detection of cytokine secretion cells were coated with capture antibodies for IL-10 and TNFα (Miltenyi Biotec) prior to macrophage stimulation. After stimulation cells from bulk or droplet cultures were collected and stained with Zombie NIR™ (Biolegend) at a final dilution of 1:2.000 to check viability. After washing cells were stained using an antibody cocktail of the following fluorescent antibodies: anti-Human cluster of differentiation 80 (CD80)- APC-R700 (BD Bioscience), anti-Human C-C chemokine receptor 7 (CCR7) - Brilliant violet 421™, anti-Human CD206- PE/Cy7, anti-Human CD200R- PE/Dazzle™ 594, (all from Biolegend), anti-human TNFα-APC and anti-human IL-10-PE (both from Miltenyi Biotec). Flow cytometric analysis was performed using FACScanto II or FACSaria III (both from BD bioscience). Results were analyzed using FlowJo (FlowJo LLC). Marker expression was quantified using median fluorescent intensity (MFI).
Tiemeijer B.M., Heester S., Sturtewagen A.Y., Smits A.I, & Tel J. (2023). Single-cell analysis reveals TLR-induced macrophage heterogeneity and quorum sensing dictate population wide anti-inflammatory feedback in response to LPS. Frontiers in Immunology, 14, 1135223.
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Publication 2023
Antibodies Cells Chemokine Receptor Combined Antibody Therapeutics Cytokine Dietary Fiber Flow Cytometry Fluorescent Antibody Technique Homo sapiens IL10 protein, human Macrophage secretion Technique, Dilution Tumor Necrosis Factor-alpha Viola
4
Lyophilized Antibody Cocktail for Flow Cytometry Staining
To minimize batch to batch variability across sites during sample processing, we used a lyophilized antibody cocktail consisting of eight premixed antibodies that was fabricated and lyophilized for the flow cytometry staining panel used in this study (BioLegend, San Diego, CA). Because the final panel consisted of three antibodies containing brilliant violet technology, one of these antibodies was added in the appropriate concentration after the lyophilized cocktail was resuspended with appropriate stabilization buffers (BD Biosciences, Franklin Lake, NJ). We included a live/dead stain to allow gating on live cells in the analysis. The composition of the lyophilized cocktail was as follows: CD4 (clone OKT4) FITC, CD3 (clone SK7) Alexa Fluor700, CD45RA (clone HI100) APC/Fire760, CD127 (clone A019D6) PE, CD25 (clone BC96) PE/Cyaine7, CD194/CCR4 (cloneL291H4) APC, CD183/CXCR3 (clone G026H7) Brilliant Violet 421, CD45RO (clone UCHL1) Brilliant Violet 711, CD196 (CCR6) (clone G03E3) PE/Dazzle 594.
We also designed a separate lyophilized cocktail that we included with each sample to serve as the fluorescence minus one (FMO) control for CCR4, CCR6 and CXCR3. This cocktail included all antibodies listed above except these three chemokine receptors. The appropriate concentration of each antibody (minus one) was added to each FMO control using separate liquid reagents for CCR4, CCR6 and CXCR3.
Magallon R.E., Harmacek L.D., Arger N.K., Grewal P., Powers L., Werner B.R., Barkes B.Q., Li L., MacPhail K., Gillespie M., White E.K., Collins S.E., Brown T., Cardenas J., Chen E.S., Maier L.A., Leach S.M., Hamzeh N.Y., Koth L.L, & O’Connor B.P. (2023). Standardization of flow cytometry and cell sorting to enable a transcriptomic analysis in a multi-site sarcoidosis study. PLOS ONE, 18(3), e0281210.
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Publication 2023
Antibodies Buffers CCR6 protein, human CD45RO Antigens Cells Chemokine Receptor Clone Cells Combined Antibody Therapeutics CXCR3 protein, human Flow Cytometry Fluorescein-5-isothiocyanate Fluorescence IL2RA protein, human Immunoglobulins Stains UCHL1 protein, human Viola
5
Basophil Activation Test for Remibrutinib
To study basophil activation, Flow CAST® BAT was used following manufacturer's instructions. In these experiments, blood from healthy donors was incubated with or without 1 μM remibrutinib for 1 h at 37°C before the addition of controls' and patients' sera (10%). In each experiment, a negative control consisting of unstimulated blood and a positive control (blood stimulated with anti‐FcɛR1 monoclonal antibodies [mAb] to crosslink the receptor) were included. After an additional 30 min of incubation with the sera at 37°C, blood cells were stained with anti‐CD193 (chemokine receptor 3, CCR3)‐PE and the anti‐CD63‐fluorescein (FITC) included in the staining reagent of the kit. Finally, red blood cells were lysed, and samples were analyzed by flow cytometry.
Gimeno R., Ribas‐Llauradó C., Pesque D., Andrades E., Cenni B., Ambros B., Pujol R, & Giménez‐Arnau A.M. (2023). Remibrutinib inhibits hives effector cells stimulated by serum from chronic urticaria patients independently of FcεR1 expression level and omalizumab clinical response. Clinical and Translational Allergy, 13(3), e12227.
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Publication 2023
Basophils BLOOD Blood Cells CCR3 protein, human CD3EAP protein, human Chemokine Receptor Donor, Blood Erythrocytes Flow Cytometry Fluorescein Fluorescein-5-isothiocyanate Monoclonal Antibodies Patients remibrutinib Serum

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1
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10
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More about "Chemokine Receptor"

Chemokine Receptors, also known as C-C Motif Chemokine Receptors (CCRs) or CXC Chemokine Receptors (CXCRs), are a family of cell surface proteins that bind to chemokines, a class of small cytokines that regulate cell trafficking and migration.
These G protein-coupled receptors (GPCRs) play a crucial role in various physiological and pathological processes, including immune responses, inflammation, and cancer metastasis.
Chemokine Receptors activate signal transduction pathways upon ligand binding, leading to changes in cellular behavior.
Studying these receptors is essential for understanding the mechanisms underlying immune system function and developing potential therapeutic interventions for a wide range of diseases, such as autoimmune disorders, infectious diseases, and cancer.
Researchers can leverage tools like the TRIzol reagent, RNeasy Mini Kit, and GolgiStop to isolate and analyze Chemokine Receptor expression and function.
Flow cytometry techniques, using instruments like the LSRFortessa, FACSCanto II, and FACSCalibur, can be employed to quantify and characterize Chemokine Receptor-expressing cells.
Additionally, the use of Ionomycin and the Cytofix/Cytoperm kit can be helpful in studying Chemokine Receptor-mediated signaling and cellular responses.
The PubCompare.ai platform can streamline the research process by providing access to the best protocols from literature, preprints, and patents, while leveraging AI-driven comparisons to ensure reproducible and accurate results.
This enables researchers to make more informed decisions and optimize their Chemokine Receptor research.