Chemokines
Chemokines, CXC
Chemokines, CC
Receptors, Chemokine
Chemokine CCL5
Chemokine CXCL10
Chemokines, C
Macrophage Inflammatory Proteins
Chemokine CCL2
Chemokine CCL4
Chemokine CXCL1
Chemokine CCL3
Chemokines, CX3C
Chemokine CXCL11
Cytokines
Chemokine CCL7
Monocyte Chemoattractant Proteins
Chemokine CXCL2
Chemotaxis, Leukocyte
Receptors, Interleukin-8B
Chemokine CXCL5
Interleukin-8
Duffy Blood-Group System
Receptors, CXCR3
Chemokine CCL19
Chemokine CCL21
Chemotactic Factors
Chemokine CCL17
Receptors, CCR2
Chemokine CCL8
Receptors, CCR1
Chemokine CCL11
Chemokine CXCL12
Monokines
Chemotaxis
Inflammation
Chemokine CCL22
Receptors, Interleukin-8A
Cells, Cultured
Chemokine CCL1
Chemokine CCL24
Receptors, CCR5
Cell Movement
Chemokine CXCL6
Chemokine CX3CL1
Receptors, CCR3
RNA, Messenger
Inflammation Mediators
Receptors, CXCR4
Neutrophil Infiltration
Receptors, CCR10
Intercellular Signaling Peptides and Proteins
Chemokine CXCL13
Neutrophils
Monocytes
Chemokine CCL20
Leukocytes
Receptors, Cytokine
Macrophages
Signal Transduction
Mice, Knockout
T-Lymphocytes
Gene Expression Regulation
Receptors, CCR7
beta-Thromboglobulin
Receptors, CCR4
Tumor Necrosis Factor-alpha
Up-Regulation
Lung
Interferon-gamma
Reverse Transcriptase Polymerase Chain Reaction
Dendritic Cells
Enzyme-Linked Immunosorbent Assay
Immunity, Innate
NF-kappa B
Receptors, CCR8
Disease Models, Animal
Lipopolysaccharides
Flow Cytometry
Platelet Factor 4
Receptors, CCR6
Eosinophils
Th2 Cells
Chemotactic Factors, Eosinophil
Th1 Cells
Gene Expression
Epithelial Cells
Ligands
Receptors, CXCR5
Gene Expression Profiling
Leukocytes, Mononuclear
Chemokine CCL27
Bronchoalveolar Lavage Fluid
Growth Substances
Cell Migration Inhibition
Neutrophil Activation
Intercellular Adhesion Molecule-1
Immunohistochemistry
Molecular Sequence Data
Endothelial Cells
Oligonucleotide Array Sequence Analysis
Cell Adhesion Molecules
Interleukin-6
Receptors, Interleukin
CD4-Positive T-Lymphocytes
Lymphocyte Activation
Receptors, Cell Surface
Interleukin-1beta
Toll-Like Receptors
Interleukin-1
Mice, Transgenic
Amino Acid Sequence
Endothelium, Vascular
Skin
Lymphocytes
Leukocyte Rolling
Cell Communication
Microglia
Vascular Cell Adhesion Molecule-1
Biological Markers
Antigens, CD
Culture Media, Conditioned
Macrophages, Alveolar
Down-Regulation
Lymphoid Tissue
Protein Binding
Coculture Techniques
Interleukins
Models, Immunological
Receptors, HIV
Lymph Nodes
Angiostatic Proteins
CD8-Positive T-Lymphocytes
Stromal Cells
Neovascularization, Pathologic
Interleukin-17
Fibroblasts
Macrophage Activation
HIV-1
Cell Differentiation
Lymphotoxin-beta
Toll-Like Receptor 4
Receptors, Interleukin-17
Integrin alpha4beta1
Respiratory Mucosa
Synovial Membrane
Real-Time Polymerase Chain Reaction
Arthritis, Rheumatoid
Toll-Like Receptor 2
Mast Cells
Glycosaminoglycans
T-Lymphocyte Subsets
Astrocytes
Interleukin-1alpha
Interleukin-10
Killer Cells, Natural
Toll-Like Receptor 3
Allergens
Endothelium, Lymphatic
Chemokine mRNA expression in gastric mucosa is associated with Helicobacter pylori cagA positivity and severity of gastritis. (1/4853)
AIM: To investigate the association between the quantity of gastric chemokine mRNA expression, severity of gastritis, and cagA positivity in Helicobacter pylori associated gastritis. METHODS: In 83 dyspeptic patients, antral and corpus biopsies were taken for semiquantitative reverse transcription polymerase chain reaction (RT-PCR) and histological grading of gastritis. Gastritis was evaluated by visual analogue scales. Quantities of chemokine (IL-8, GRO alpha, ENA-78, RANTES, MCP-1) RT-PCR products were compared with G3PDH products. Each sample was also evaluated for the presence of cagA and ureA mRNA by RT-PCR. RESULTS: mRNA expression of all five chemokines was significantly greater in H pylori positive than in H pylori negative mucosa. In H pylori positive patients, in the antrum C-X-C chemokine mRNA expression was significantly greater in cagA positive patients than in cagA negative patients, but there were no significant differences in C-C chemokine mRNA expression. In H pylori positive patients, chemokine mRNA expression in the corpus was less than in the antrum. In contrast to the antrum, only GRO alpha mRNA expression was significantly greater in cagA positive infection. Polymorphonuclear cell infiltration was correlated with C-X-C chemokine mRNA expression. Significant correlations were also found between bacterial density and C-X-C chemokine mRNA expression. CONCLUSIONS: In H pylori infection, C-X-C chemokines may play a primary role in active gastritis. Infection with cagA positive H pylori induces greater gastric chemokine mRNA expression in the antral mucosa, which may be relevant to the increased mucosal damage associated with cagA positive H pylori infection. (+info)Isolation of novel GRO genes and a phylogenetic analysis of the CXC chemokine subfamily in mammals. (2/4853)
Approximately 15 different alpha, or CXC, chemokines have thus far been isolated from 11 species of mammals. Among the best studied chemokines are the 12 human proteins that are encoded by 11 paralogous genes. In order to better understand the evolution and function of this group of genes, we isolated and characterized six novel GRO and GRO-related cDNA sequences from the cow (Bos taurus), the sheep (Ovis aries), the rabbit (Oryctolagus cuniculus), and the guinea pig (Cavia porcellus). The amino acid sequence of the diverged guinea pig GRO or KC gene is only 50%-60% similar to presumed orthologs from other species, while the sheep and cow GRO proteins are 90%-99% similar to each other. The presence of multiple GRO genes in the cow, the rabbit, and the sheep is consistent with what has been observed for humans. Phylogenetic analyses of amino acid sequences from 44 proteins indicate that genes orthologous to many of the 11 known from humans exist in other species. One such gene, interleukin 8, or IL8, has been isolated from nine species, including the rodent guinea pig; however, this gene is absent in the rat and the mouse, indicating a unique gene loss event in the rat/mouse (muroid rodent) lineage. The KC (or MIP2) gene of rodents appears to be orthologous to the GRO gene found in other taxonomic orders. Combined evidence from different sources suggests that IP10 and MIG share sister taxon relationships on the evolutionary tree, while the remaining paralogous genes represent independent lineages, with limited evidence for kinship between them. This observation indicates that these genes originated nearly contemporaneously via a series of gene duplication events. Relative-rate tests for synonymous and nonsynonymous nucleotide substitutions in the KC and IL8 genes did not detect rate heterogeneity; however, there are several notable features regarding the IL8 genes. For example, the IL8 proteins from two Old World monkeys are as similar to one another as they are to the IL8 protein from humans, and all observed nucleotide differences between the IL8 genes of the two monkeys cause amino acid changes; in other words, there are no synonymous differences between them. (+info)Selective recruitment of CCR4-bearing Th2 cells toward antigen-presenting cells by the CC chemokines thymus and activation-regulated chemokine and macrophage-derived chemokine. (3/4853)
Helper T cells are classified into Th1 and Th2 subsets based on their profiles of cytokine production. Th1 cells are involved in cell-mediated immunity, whereas Th2 cells induce humoral responses. Selective recruitment of these two subsets depends on specific adhesion molecules and specific chemoattractants. Here, we demonstrate that the T cell-directed CC chemokine thymus and activation-regulated chemokine (TARC) was abundantly produced by monocytes treated with granulocyte macrophage colony stimulating factor (GM-CSF) or IL-3, especially in the presence of IL-4 and by dendritic cells derived from monocytes cultured with GM-CSF + IL-4. The receptor for TARC and another macrophage/dendritic cell-derived CC chemokine macrophage-derived chemokine (MDC) is CCR4, a G protein-coupled receptor. CCR4 was found to be expressed on approximately 20% of adult peripheral blood effector/memory CD4+ T cells. T cells attracted by TARC and MDC generated cell lines predominantly producing Th2-type cytokines, IL-4 and IL-5. Fractionated CCR4+ cells but not CCR4- cells also selectively gave rise to Th2-type cell lines. When naive CD4+ T cells from adult peripheral blood were polarized in vitro, Th2-type cells selectively expressed CCR4 and vigorously migrated toward TARC and MDC. Taken together, CCR4 is selectively expressed on Th2-type T cells and antigen-presenting cells may recruit Th2 cells expressing CCR4 by producing TARC and MDC in Th2-dominant conditions. (+info)Prospects for cytokine and chemokine biotherapy. (4/4853)
Cytokines with immunostimulating effects have the capacity to induce tumor immunity in animal models, whereas some cytokines interfere with tumor growth based on their angiostatic effects. Despite these capabilities, cytokines, such as IFN-, IFN-, tumor necrosis factor, interleukin (IL)-1, and IL-2, have had limited clinical efficacy and many undesirable side effects. In preclinical models, cytokines can even promote tumor growth and increase metastatic spread. Although chemokines have had limited clinical evaluation, studies of animal models show that they can also have tumor-suppressive or tumor-enhancing effects. In mice, chemokines, such as IP-10, RANTES, and TCA3, have resulted in tumor regression and immunity to subsequent tumor challenge. Those chemokines that are angiostatic (e.g., PF4, IP-10, and MIG) can also induce tumor regression by reducing the tumor blood supply. Conversely, IL-8, which is angiogenic, can promote tumor growth. Our studies show that nasopharyngeal cell line cells (FADU) show a chemotactic as well as a proliferative response to MCP-1. In addition, a variant murine T cell lymphoma cell line Esb-MP, unlike the parental variant Esb, was selectively chemoattracted by murine MCP-1/JE. When injected s.c. into mice, the Esb-MP variant metastasized to the kidney with much higher frequency than the Esb variant. Both cultured kidneys from normal mice and a mesangial cell line constitutively produced chemoattractants that acted on Esb-MP but not Esb parental cells. Purification to homogeneity of these chemoattractants led to the identification of RANTES and JE. These results demonstrate that some chemokines may promote tumor growth and organ-specific metastatic spread of those tumors that have adapted and become responsive to chemokines. Finally, tumors appear to use numerous adaptive mechanisms to subvert and suppress the immune system. More effective therapy with cytokines and chemokines will require better characterization of the means by which tumors develop resistance to cytokines and overcome the immune system. Only then can we develop appropriate therapeutic approaches to antagonize cancer-induced immunosuppression. (+info)Persistent chlamydial envelope antigens in antibiotic-exposed infected cells trigger neutrophil chemotaxis. (5/4853)
An in vitro coculture model system was used to explore conditions that trigger neutrophil chemotaxis to Chlamydia trachomatis infected human epithelial cells (HEC-1B). Polarized HEC-1B monolayers growing on extracellular matrix (ECM) were infected with C. trachomatis serovar E. By 36 h, coincident with the secretion of chlamydial lipopolysaccharide and major outer membrane protein to the surfaces of infected cells, human polymorphonuclear neutrophils (PMNL) loaded with azithromycin migrated through the ECM and infiltrated the HEC-1B monolayer. Bioreactive azithromycin was delivered by the chemotactic PMNL to infected epithelial cells in concentrations sufficient to kill intracellular chlamydiae. However, residual chlamydial envelopes persisted for 4 weeks, and PMNL chemotaxis was triggered to epithelial cells containing residual envelopes. Infected endometrial cells demonstrated up-regulation of ENA-78 and GCP-2 chemokine mRNA. Thus, despite appropriate antimicrobial therapy, residual chlamydial envelope antigens may persist in infected tissues of culture-negative women and provide one source for sustained inflammation. (+info)Mechanisms of acute inflammatory lung injury induced by abdominal sepsis. (6/4853)
Sequestration of neutrophils and release of histotoxic mediators are considered important for the development of pathologic alterations of the lung defined as adult respiratory distress syndrome. Mechanisms of inflammatory lung injury caused by abdominal sepsis were investigated using the colon ascendens stent peritonitis (CASP) model that closely mimics the human disease. In the CASP model, a continuous leakage of intraluminal bacteria into the peritoneal cavity is induced by implantation of a stent in the ascending colon, generating a septic focus. In contrast to the cecal ligation and puncture model of peritonitis, survival of mice following CASP surgery is dependent on IFN-gamma, but independent of tumor necrosis factor (TNF). Here we show that the systemic inflammation induced by CASP surgery results in a rapid and profound increase of lung vascular permeability that was associated with the activation and recruitment of neutrophils to the lung. Activation of circulating granulocytes was characterized by increased production of serine proteinases and reactive oxygen metabolites, as well as elevated expression of cell surface Mac-1. Expression of MIP-2, KC, MIP-1alpha and E-selectin mRNA in lung was strongly increased within 3 h following CASP surgery, whereas up-regulation of IP-10, MCP-1 and P-selectin was delayed. In contrast, induction of RANTES, LIX, ICAM-1 and VCAM-1 mRNA was weak or not detectable after CASP surgery. Importantly, recruitment of leukocytes to the lung was normal in lipopolysaccharide-resistant mice, and was not affected by antibody neutralization of TNF or the chemokines MIP-2 and KC. (+info)Chemokine expression in CF epithelia: implications for the role of CFTR in RANTES expression. (7/4853)
To delineate the mechanisms that facilitate leukocyte migration into the cystic fibrosis (CF) lung, expression of chemokines, including interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1), and RANTES, was compared between CF and non-CF airway epithelia. The findings presented herein demonstrate that, under either basal conditions or tumor necrosis factor-alpha (TNF-alpha)- and/or interferon-gamma (IFN-gamma)-stimulated conditions, a consistent pattern of differences in the secretion of IL-8 and MCP-1 between CF and non-CF epithelial cells was not observed. In contrast, CF epithelial cells expressed no detectable RANTES protein or mRNA under basal conditions or when stimulated with TNF-alpha and/or IFN-gamma (P +info)Cutting edge: clustered AU-rich elements are the target of IL-10-mediated mRNA destabilization in mouse macrophages. (8/4853)
In the present study we show that IL-10-mediated inhibition of inflammatory gene expression can be mediated by an AU-rich element (ARE) cluster present in the 3' untranslated region (3'UTR) of sensitive genes. A series of chloramphenicol acetyl transferase (CAT) reporter gene constructs were prepared in which different fragments from the IL-10-sensitive KC mRNA 3'UTR were placed downstream of the coding region of the reporter gene CAT. CAT mRNA containing the KC 3'UTR was markedly destabilized as compared with the control CAT mRNA, and the decay rate was further increased in cells stimulated with IL-10. The KC 3'UTR contains an ARE cluster and three isolated ARE motifs. The ARE cluster spanning nucleotides 378-399 appeared to be both necessary and sufficient to mediate sensitivity to IL-10 because a 116-nucleotide fragment that contains the cluster conferred sensitivity, while mutation of the sequence between positions 378 and 399 eliminated sensitivity. The destabilizing effect of IL-10 was relatively selective, as the stability of chimeric CAT mRNAs was not modulated in cells treated with IFN-gamma or IL-4. (+info)There are several key features of inflammation:
1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.
Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.
There are several types of inflammation, including:
1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.
There are several ways to reduce inflammation, including:
1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.
It's important to note that chronic inflammation can lead to a range of health problems, including:
1. Arthritis
2. Diabetes
3. Heart disease
4. Cancer
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.
Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
Pathologic neovascularization can be seen in a variety of conditions, including cancer, diabetic retinopathy, and age-related macular degeneration. In cancer, for example, the formation of new blood vessels can help the tumor grow and spread to other parts of the body. In diabetic retinopathy, the growth of new blood vessels in the retina can cause vision loss and other complications.
There are several different types of pathologic neovascularization, including:
* Angiosarcoma: a type of cancer that arises from the cells lining blood vessels
* Hemangiomas: benign tumors that are composed of blood vessels
* Cavernous malformations: abnormal collections of blood vessels in the brain or other parts of the body
* Pyogenic granulomas: inflammatory lesions that can form in response to trauma or infection.
The diagnosis of pathologic neovascularization is typically made through a combination of physical examination, imaging studies (such as ultrasound, CT scans, or MRI), and biopsy. Treatment options vary depending on the underlying cause of the condition, but may include medications, surgery, or radiation therapy.
In summary, pathologic neovascularization is a process that occurs in response to injury or disease, and it can lead to serious complications. It is important for healthcare professionals to be aware of this condition and its various forms in order to provide appropriate diagnosis and treatment.
Symptoms of pneumonia may include cough, fever, chills, difficulty breathing, and chest pain. In severe cases, pneumonia can lead to respiratory failure, sepsis, and even death.
There are several types of pneumonia, including:
1. Community-acquired pneumonia (CAP): This type of pneumonia is caused by bacteria or viruses and typically affects healthy people outside of hospitals.
2. Hospital-acquired pneumonia (HAP): This type of pneumonia is caused by bacteria or fungi and typically affects people who are hospitalized for other illnesses or injuries.
3. Aspiration pneumonia: This type of pneumonia is caused by food, liquids, or other foreign matter being inhaled into the lungs.
4. Pneumocystis pneumonia (PCP): This type of pneumonia is caused by a fungus and typically affects people with weakened immune systems, such as those with HIV/AIDS.
5. Viral pneumonia: This type of pneumonia is caused by viruses and can be more common in children and young adults.
Pneumonia is typically diagnosed through a combination of physical examination, medical history, and diagnostic tests such as chest X-rays or blood tests. Treatment may involve antibiotics, oxygen therapy, and supportive care to manage symptoms and help the patient recover. In severe cases, hospitalization may be necessary to provide more intensive care and monitoring.
Prevention of pneumonia includes vaccination against certain types of bacteria and viruses, good hygiene practices such as frequent handwashing, and avoiding close contact with people who are sick. Early detection and treatment can help reduce the risk of complications and improve outcomes for those affected by pneumonia.
There are several symptoms of RA, including:
1. Joint pain and stiffness, especially in the hands and feet
2. Swollen and warm joints
3. Redness and tenderness in the affected areas
4. Fatigue, fever, and loss of appetite
5. Loss of range of motion in the affected joints
6. Firm bumps of tissue under the skin (rheumatoid nodules)
RA can be diagnosed through a combination of physical examination, medical history, blood tests, and imaging studies such as X-rays or ultrasound. Treatment typically involves a combination of medications, including nonsteroidal anti-inflammatory drugs (NSAIDs), disease-modifying anti-rheumatic drugs (DMARDs), and biologic agents. Lifestyle modifications such as exercise and physical therapy can also be helpful in managing symptoms and improving quality of life.
There is no cure for RA, but early diagnosis and aggressive treatment can help to slow the progression of the disease and reduce symptoms. With proper management, many people with RA are able to lead active and fulfilling lives.
Chemokine
Chemokine receptor
CXC chemokine receptors
CC chemokine receptors
Broad-spectrum chemokine inhibitor
C-c motif chemokine ligand 27
C-C chemokine receptor type 6
C-C chemokine receptor type 7
C-C motif chemokine ligand 24
C-C motif chemokine ligand 3 like 3
Family with sequence similarity 19 (chemokine (C-C motif)-like), member A1
Family with sequence similarity 19 member A4, C-C motif chemokine like
CCL7
CCL1
G protein-coupled receptor
Alberto Mantovani
CCL2
Marco Baggiolini
CCR5 receptor antagonist
CCL11
Immune system
Neuroinflammation
Clare Lloyd
Lymph node stromal cell
Colostrum
Macrophage
Victoria A. Harden
CCR2
Interleukin 8 receptor, alpha
CXCR6
Human Cytokines, Growth Factors & Chemokines from RDI
Figure - Chemokine Receptor 5 Δ32 Allele in Patients with Severe Pandemic (H1N1) 2009 - Volume 16, Number 10-October 2010 -...
What is the definition of Chemokine receptors? | Dictionary.net
ELEVATED PRODUCTION OF NOCICEPTIVE CC-CHEMOKINES AND SE-SELECTIN IN PATIENTS WITH LOW BACK PAIN AND THE EFFECTS OF SPINAL...
Chemokine CX3CL1 | Scholars@Duke
Recombinant Rat C-C motif chemokine protein (Ccl28) (Active) | CSB-AP001601RA | Cusabio
Schistosoma mansoni secretes a chemokine binding protein with antiinflammatory activity - White Rose Research Online
Rat Cytokine/Chemokine Immunoassay Panel
"Chemokines in the corpus luteum: implications of leukocyte chemotaxis" by David H. Townson and Amy R. Liptak
"Chemokine-opioid Interaction as a Potential Target for Addiction and P" by Megan Hrinda
Mitochondrial reactive oxygen species regulate the induction of CD8+ T cells by plasmacytoid dendritic cells | Nature...
elisa kits for chemokines - NF-κB
elisa kits for chemokines - Cholera toxin
Chemokine CCL5 | Profiles RNS
Chemokine CCL5
- McMaster Experts
Chemokine CXCL4 interactions with extracellular matrix proteoglycans mediate widespread immune cell recruitment independent of...
Canonical and atypical chemokine receptors in the neutrophil life cycle. | Cytokine;169: 156297, 2023 09. | MEDLINE
CC chemokines and receptors in osteoarthritis: new insights and potential targets. | Arthritis Res Ther;25(1): 113, 2023 07 03...
Repositório Institucional da Universidade de Aveiro: Chemokines impact in Alzheimer's disease
Mouse MDC(Macrophage Derived Chemokine) ELISA Kit - Gencyst
Polyclonal Antibody to Macrophage Derived Chemokine (MDC) - danabio
Carina Biotech's proprietary multifunctional chemokine receptor platform - Carina Biotech
T cells and their partners: The chemokine dating agency
Recombinant Human C-C chemokine receptor type 4(CCR4)-VLPs (Active) - Cusabio
Appendices of the 1997 Genomics Strategic Plan | CDC
Chemokines certainly are a grouped category of chemotactic cytokines that play - EGFR Inhibitors in lung cancer
Chemokine-Releasing Microparticles Improve Bacterial Clearance and Survival of Anthrax Spore-Challenged Mice
PGS Catalog - PGS000220 / C-C motif chemokine 20 (CCL20) serum levels (Polygenic Score)
Receptors17
- PURPOSE This solicitation invites research grant applications focused on the role of chemokines and chemokine receptors in the lungs, cardiovascular system and bone marrow to elucidate virus-cell interactions in the pathogenesis of HIV in the pulmonary, cardiovascular and hematopoietic systems. (nih.gov)
- Another facet of the initiative is to determine if potential new antiviral agents, based on the molecular interactions between chemokines, their receptors and virus, block infection of cells in the lungs, cardiovasculature and bone marrow or alter the evolution of virus in the involved organs. (nih.gov)
- This RFA, HIV in the Lungs, Heart, and Blood: Role of Chemokines and Their Receptors, is related to the priority areas of HIV infection and immunization and infectious diseases. (nih.gov)
- Chemokines are a physiological system that is finely tuned by ligand and receptor expression, ligand or receptor oligomerization, redundancy, expression of atypical receptors, and non-GPCR binding partners that cumulatively influence discrete pharmacological signaling responses and cellular functions. (nih.gov)
- What is the definition of Chemokine receptors? (dictionary.net)
- Here we show that S. mansoni eggs secrete a protein into host tissues that binds certain chemokines and inhibits their interaction with host chemokine receptors and their biological activity. (whiterose.ac.uk)
- Tumor cell invasion share many similarities with leukocyte trafficking, which is critically regulated by chemokines and their receptors. (oncotarget.com)
- Chemokine receptors are cytokine receptors found on the surface of certain cells that interact with a type of cytokine called a chemokine. (oncotarget.com)
- There have been 19 distinct chemokine receptors in mammals. (oncotarget.com)
- Following interaction with their specific chemokine ligands, chemokine receptors trigger a flux in intracellular calcium (Ca2+) ions (calcium signaling). (oncotarget.com)
- It also encodes a collection of chemokine receptors, which play a role in the immune response in the airways of our lungs. (nih.gov)
- Chemokine receptor antagonists inhibit chemokine receptors expressed on cancer and stromal cells. (multiplemyelomahub.com)
- Canonical and atypical chemokine receptors in the neutrophil life cycle. (bvsalud.org)
- Atypical chemokine receptors (ACKRs) are regulators of the chemokine system by controlling chemokine bioavailability and chemokine receptor function. (bvsalud.org)
- The aim of this review is to give an overview of the current evidence regarding the role of chemokines and chemokine receptors in the life of neutrophils with a focus on the regulation exerted by ACKRs. (bvsalud.org)
- CC chemokines and receptors in osteoarthritis: new insights and potential targets. (bvsalud.org)
- Due to the local inflammation , the expression of various cytokines was altered in affected joints , including CC motif chemokine ligands (CCLs) and their receptors (CCRs). (bvsalud.org)
Cytokines and chemokines6
- Research Diagnostics Inc (RDI) offers a wide line of recombinant growth factors, cytokines and chemokines (new products added throughout year, please inquire if not listed below). (researchd.com)
- This kit may be used for the analysis of the above cytokines and chemokines in rat serum, plasma, other rat biological fluids, tissue/ cell extracts, or cell culture supernatants. (lincoresearch.com)
- Downregulation of Cytokines and Chemokines by GB Virus C After Transmission Via Blood Transfusion in HIV-Positive Blood Recipients. (nih.gov)
- Most of the modulated cytokines and chemokines were reduced after GBV-C detection, including many proinflammatory cytokines, suggesting an overall antiinflammatory effect of GBV-C in HIV-positive subjects. (nih.gov)
- Hepatocytes, as well as nonparenchymal cells, secrete proinflammatory cytokines and chemokines that are involved in the pathology of many liver diseases. (cdc.gov)
- Taken together these studies indicate that, in addition to other inflammatory mediators and acute phase proteins, cytokines and chemokines are produced by hepatocytes, which may participate in hepatotoxic responses. (cdc.gov)
CCL53
- Chemokine CCL5" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (wakehealth.edu)
- This graph shows the total number of publications written about "Chemokine CCL5" by people in this website by year, and whether "Chemokine CCL5" was a major or minor topic of these publications. (wakehealth.edu)
- Below are the most recent publications written about "Chemokine CCL5" by people in Profiles. (wakehealth.edu)
Leukocyte recruitment1
- Chemokines are chemotactic cytokines, leads to leukocyte recruitment and activation. (multiplemyelomahub.com)
Receptor antagonists1
- Next steps include continuing to investigate RAP-103 and other multi-chemokine receptor antagonists or agonists. (conncoll.edu)
Chemotactic2
Macrophage inflamm1
- In particular, tumor necrosis factor-alpha (TNFalpha), as well as members of the CXC family of chemokines, including interleukin (IL)-8 in humans and macrophage inflammatory protein (MIP)-2 in rodents, have been implicated in both damage and repair processes associated with various hepatotoxins. (cdc.gov)
Protein2
- The purified recombinant S. mansoni chemokine binding protein (smCKBP) suppressed inflammation in several disease models. (whiterose.ac.uk)
- smCKBP is unrelated to host proteins and is the first described chemokine binding protein encoded by a pathogenic human parasite and may have potential as an antiinflammatory agent. (whiterose.ac.uk)
Proteins2
- The chemokine system, which is a signaling system using small proteins called chemokines, helps to regulate the release of dopamine in the mesolimbic system, which is the primary neurotransmitter in reward behavior. (conncoll.edu)
- Was found that hNGFp acts on glial cells, modulating inflammatory proteins such as the soluble TNFa receptor II and the chemokine CXCL12. (nih.gov)
Proinflammatory1
- The mouse provides a model to investigate the function of the chemokine receptor CX3CR1, which is a proinflammatory receptor for the leukocyte chemoattractant CX3CL1 (aka fractalkine). (nih.gov)
CCR52
Molecules3
- and determining whether the cell signaling specific to the dual presence of DARC and the chemokine receptor is regulated by the molecules. (nih.gov)
- Cell surface glycoproteins that bind to chemokines and thus mediate the migration of pro - inflammatory molecules. (dictionary.net)
- It binds cell-signaling molecules called chemokines (e.g. (cdc.gov)
Tissues2
- Chemokines are small Molecular weight peptides responsible for adhesion, activation, and recruitment of leukocytes into tissues. (unh.edu)
- Due to the redundancy and pleiotropicity of the chemokine system, chemokines have often multiple and complex roles in neutrophil differentiation ranging from retention and control of proliferation of progenitors to the mobilization of mature cells from the bone marrow (BM) to the bloodstream and their further differentiation in tissues . (bvsalud.org)
Chemotaxis2
- Information about the role of chemokines and leukocyte trafficking (chemotaxis) during ovarian function is important to understanding paracrine-autocrine relationships shared between reproductive and immune systems. (unh.edu)
- While Card9-/- neutrophils showed no cell-intrinsic chemotaxis defect in mixed bone marrow chimera experiments, the induction of neutrophil-recruiting chemokines was significantly impaired in infected Card9-/- brains, from myeloid and non-myeloid cellular sources. (nih.gov)
Tumor1
- In cancer, chemokines play paradoxical roles in both the directed emigration of metastatic, receptor-expressing cancer cells out of the tumor as well as immigration of tumor-infiltrating immune cells that culminate in a tumor-unique immune microenvironment. (nih.gov)
Immune1
- The laboratory has established hair follicles as immunologically functional structures that recruit and control the localization of immune cells through the production of chemokines and cytokines. (nih.gov)
Serum1
- Serum, plasma, or urine chemokine levels are assessed using 50 ul frozen specimen per sandwich ELISA in duplicate using the appropriate commercially-available capture antibodies, detection antibodies, and standard ELISA reagents (R&D Systems), as we have described previously (15, 17, 18). (nih.gov)
Neutrophil2
- Thus, CARD9 is critical for control of fungal invasion in the CNS, acting to promote neutrophil trafficking via production of neutrophil-targeted chemokines. (nih.gov)
- Even though ACKRs bind a wide range of chemokines , they appear to have a selective role in the process of neutrophil production and differentiation. (bvsalud.org)
Gene expression1
- Using human Hep G2 cells and freshly isolated rodent hepatocytes, it was demonstrated that metals increase gene expression and secretion of CXC chemokines and TNFalpha. (cdc.gov)
Infection2
- An important aspect of this RFA is to determine if chemokines or their derivatives can effectively block infection of tissue macrophages and macrophage-lymphocyte transfer of virus. (nih.gov)
- Human studies, e.g., in subjects with various chemokine receptor phenotypes, or with varying stages of HIV infection as compared to healthy persons, and studies in animal models would be of interest. (nih.gov)
Cells1
- The both studied chemokines resulted in small alterations regarding the cytotoxicity on SH-SY5Y differentiated cells, being a significant increase in apoptosis observed only for the MCP-1 at the highest concentration. (ua.pt)
Role1
- As essential members of chemokines , CCLs and CCRs played an important role in the pathogenesis and treatment of OA. (bvsalud.org)
Effectively1
- In the age of precision oncology, strategies to effectively harness the power of immunotherapy requires consideration of chemokine gradients within the unique spatial topography and temporal influences with heterogeneous tumors. (nih.gov)
Tissue1
- Here we report that the chemokine receptor CCR10 is highly expressed in human glioblastoma compared with control brain tissue. (oncotarget.com)
System1
- Because of this, the chemokine system is a potential target for new addiction medication research. (conncoll.edu)
Function1
- Chemokines are mainly studied for their local function in the control of leukocyte extravasation in homeostatic and inflammatory conditions. (bvsalud.org)
Expression1
- Recent advances regarding chemokine expression and leukocyte accumulation within the ovulatory follicle and the corpus luteum are the subject of this mini-review. (unh.edu)