Macrophage Inflammatory Proteins
Monocyte Chemoattractant Proteins
Duffy Blood-Group System
Intercellular Signaling Peptides and Proteins
Gene Expression Regulation
Reverse Transcriptase Polymerase Chain Reaction
Tumor Necrosis Factor-alpha
Disease Models, Animal
Enzyme-Linked Immunosorbent Assay
Platelet Factor 4
Chemotactic Factors, Eosinophil
Molecular Sequence Data
Gene Expression Profiling
Bronchoalveolar Lavage Fluid
Cell Migration Inhibition
Amino Acid Sequence
Intercellular Adhesion Molecule-1
Cell Adhesion Molecules
Oligonucleotide Array Sequence Analysis
Receptors, Cell Surface
Vascular Cell Adhesion Molecule-1
Culture Media, Conditioned
Real-Time Polymerase Chain Reaction
Toll-Like Receptor 4
Killer Cells, Natural
Dose-Response Relationship, Drug
Toll-Like Receptor 2
Toll-Like Receptor 3
Central Nervous System
Molecular uncoupling of fractalkine-mediated cell adhesion and signal transduction. Rapid flow arrest of CX3CR1-expressing cells is independent of G-protein activation. (1/163)Fractalkine is a novel multidomain protein expressed on the surface of activated endothelial cells. Cells expressing the chemokine receptor CX3CR1 adhere to fractalkine with high affinity, but it is not known if adherence requires G-protein activation and signal transduction. To investigate the cell adhesion properties of fractalkine, we created mutated forms of CX3CR1 that have little or no ability to transduce intracellular signals. Cells expressing signaling-incompetent forms of CX3CR1 bound rapidly and with high affinity to immobilized fractalkine in both static and flow assays. Video microscopy revealed that CX3CR1-expressing cells bound more rapidly to fractalkine than to VCAM-1 (60 versus 190 ms). Unlike VCAM-1, fractalkine did not mediate cell rolling, and after capture on fractalkine, cells did not dislodge. Finally, soluble fractalkine induced intracellular calcium fluxes and chemotaxis, but it did not activate integrins. Taken together these data provide strong evidence that CX3CR1, a seven-transmembrane domain receptor, mediates robust cell adhesion to fractalkine in the absence of G-protein activation and suggest a novel role for this receptor as an adhesion molecule. (+info)
Characterization of fractalkine in rat brain cells: migratory and activation signals for CX3CR-1-expressing microglia. (2/163)Molecular analyses of the chemokine fractalkine and its receptor CX3C-R1 in the rat brain have revealed a striking polarization: fractalkine is expressed constitutively in neurons and is up-regulated by TNF-alpha and IL-1beta in astrocytes. Expression of its specific receptor, CX3C-R1, is restricted to astrocytes and microglia. We have analyzed the functional correlates of this expression and demonstrate that fractalkine induces microglial cell migration and activation. However, the activity of this chemokine on astrocytes may also be highly relevant in inducing astrocyte-microglia cell interactions through cytokine/mediator release leading to microglial activation. (+info)
Inflammatory agents regulate in vivo expression of fractalkine in endothelial cells of the rat heart. (3/163)Fractalkine is distinguished structurally from other chemokines in that it contains a mucin-like stalk that tethers a CX3C chemokine module to a transmembrane-spanning region; its expression in cultured endothelial cells has been shown to be up-regulated by tumor necrosis factor alpha (TNF-alpha) and interleukin-1 (IL-1). The purpose of this study was to determine whether fractalkine is expressed, in a proinflammatory agent-regulated manner, by cardiac endothelial cells in vivo. Steady state levels of fractalkine mRNA were increased in rat cardiac tissues after in vivo treatment with lipopolysaccharide (LPS), IL-1, or TNF-alpha. In situ hybridization and immunohistochemical analysis revealed that endothelial cells of the coronary vasculature and endocardium were the principal source of proinflammatory agent-inducible fractalkine, although some fractalkine immunoreactivity was also found on the myocytes. These data are the first demonstration of in vivo cardiac endothelial cell fractalkine expression and regulation by proinflammatory agents such as LPS, IL-1, or TNF-alpha. Cardiac endothelial cell-expressed fractalkine may contribute to the influx of leukocytes into the heart during inflammation. (+info)
Neuronal fractalkine expression in HIV-1 encephalitis: roles for macrophage recruitment and neuroprotection in the central nervous system. (4/163)HIV-1 infection of the brain results in chronic inflammation, contributing to the neuropathogenesis of HIV-1 associated neurologic disease. HIV-1-infected mononuclear phagocytes (MP) present in inflammatory infiltrates produce neurotoxins that mediate inflammation, dysfunction, and neuronal apoptosis. Neurologic disease is correlated with the relative number of MP in and around inflammatory infiltrates and not viral burden. It is unclear whether these cells also play a neuroprotective role. We show that the chemokine, fractalkine (FKN), is markedly up-regulated in neurons and neuropil in brain tissue from pediatric patients with HIV-1 encephalitis (HIVE) compared with those without HIVE, or that were HIV-1 seronegative. FKN receptors are expressed on both neurons and microglia in patients with HIVE. These receptors are localized to cytoplasmic structures which are characterized by a vesicular appearance in neurons which may be in cell-to-cell contact with MPs. FKN colocalizes with glutamate in these neurons. Similar findings are observed in brain tissue from an adult patient with HIVE. FKN is able to potently induce the migration of primary human monocytes across an endothelial cell/primary human fetal astrocyte trans-well bilayer, and is neuroprotective to cultured neurons when coadministered with either the HIV-1 neurotoxin platelet activating factor (PAF) or the regulatory HIV-1 gene product Tat. Thus focal inflammation in brain tissue with HIVE may up-regulate neuronal FKN levels, which in turn may be a neuroimmune modulator recruiting peripheral macrophages into the brain, and in a paracrine fashion protecting glutamatergic neurons. (+info)
Ultrastructure and function of the fractalkine mucin domain in CX(3)C chemokine domain presentation. (5/163)Fractalkine (FKN), a CX(3)C chemokine/mucin hybrid molecule on endothelium, functions as an adhesion molecule to capture and induce firm adhesion of a subset of leukocytes in a selectin- and integrin-independent manner. We hypothesized that the FKN mucin domain may be important for its function in adhesion, and tested the ability of secreted alkaline phosphatase (SEAP) fusion proteins containing the entire extracellular region (FKN-SEAP), the chemokine domain (CX3C-SEAP), or the mucin domain (mucin-SEAP) to support firm adhesion under flow. CX3C-SEAP induced suboptimal firm adhesion of resting peripheral blood mononuclear cells, compared with FKN-SEAP, and mucin-SEAP induced no firm adhesion. CX3C-SEAP and FKN-SEAP bound to CX(3)CR1 with similar affinities. By electron microscopy, fractalkine was 29 nm in length with a long stalk (mucin domain), and a globular head (CX(3)C). To test the function of the mucin domain, a chimeric protein replacing the mucin domain with a rod-like segment of E-selectin was constructed. This chimeric protein gave the same adhesion of peripheral blood mononuclear cells as intact FKN, both when immobilized on glass and when expressed on the cell surface. This implies that the function of the mucin domain is to provide a stalk, extending the chemokine domain away from the endothelial cell surface to present it to flowing leukocytes. (+info)
Fractalkine is an epithelial and endothelial cell-derived chemoattractant for intraepithelial lymphocytes in the small intestinal mucosa. (6/163)Fractalkine is a unique chemokine that combines properties of both chemoattractants and adhesion molecules. Fractalkine mRNA expression has been observed in the intestine. However, the role of fractalkine in the healthy intestine and during inflammatory mucosal responses is not known. Studies were undertaken to determine the expression and function of fractalkine and the fractalkine receptor CX3CR1 in the human small intestinal mucosa. We identified intestinal epithelial cells as a novel source of fractalkine. The basal expression of fractalkine mRNA and protein in the intestinal epithelial cell line T-84 was under the control of the inflammatory mediator IL-1beta. Fractalkine was shed from intestinal epithelial cell surface upon stimulation with IL-1beta. Fractalkine localized with caveolin-1 in detergent-insoluble glycolipid-enriched membrane microdomains in T-84 cells. Cellular distribution of fractalkine was regulated during polarization of T-84 cells. A subpopulation of isolated human intestinal intraepithelial lymphocytes expressed the fractalkine receptor CX3CR1 and migrated specifically along fractalkine gradients after activation with IL-2. Immunohistochemistry demonstrated fractalkine expression in intestinal epithelial cells and endothelial cells in normal small intestine and in active Crohn's disease mucosa. Furthermore, fractalkine mRNA expression was significantly up-regulated in the intestine during active Crohn's disease. This study demonstrates that fractalkine-CX3CR1-mediated mechanism may direct lymphocyte chemoattraction and adhesion within the healthy and diseased human small intestinal mucosa. (+info)
Rapid progression to AIDS in HIV+ individuals with a structural variant of the chemokine receptor CX3CR1. (7/163)Human immunodeficiency virus (HIV) enters cells in vitro via CD4 and a coreceptor. Which of 15 known coreceptors are important in vivo is poorly defined but may be inferred from disease-modifying mutations, as for CCR5. Here two single nucleotide polymorphisms are described in Caucasians in CX3CR1, an HIV coreceptor and leukocyte chemotactic/adhesion receptor for the chemokine fractalkine. HIV-infected patients homozygous for CX3CR1-I249 M280, a variant haplotype affecting two amino acids (isoleucine-249 and methionine-280), progressed to AIDS more rapidly than those with other haplotypes. Functional CX3CR1 analysis showed that fractalkine binding is reduced among patients homozygous for this particular haplotype. Thus, CX3CR1-I249 M280 is a recessive genetic risk factor in HIV/AIDS. (+info)
Fractalkine-mediated endothelial cell injury by NK cells. (8/163)Endothelial cells (ECs) are primary targets of immunological attack, and their injury can lead to vasculopathy and organ dysfunction in vascular leak syndrome and in rejection of allografts or xenografts. A newly identified CX3C-chemokine, fractalkine, expressed on activated ECs plays an important role in leukocyte adhesion and migration. In this study we examined the functional roles of fractalkine on NK cell activity and NK cell-mediated endothelial cell injury. Freshly separated NK cells expressed the fractalkine receptor (CX3CR1) determined by FACS analysis and efficiently adhered to immobilized full-length fractalkine, but not to the truncated forms of the chemokine domain or mucin domain, suggesting that fractalkine functions as an adhesion molecule on the interaction between NK cells and ECs. Soluble fractalkine enhanced NK cell cytolytic activity against K562 target cells in a dose- and time-dependent manner. This enhancement correlated well with increased granular exocytosis from NK cells, which was completely inhibited by the G protein inhibitor, pertussis toxin. Transfection of fractalkine cDNA into ECV304 cells or HUVECs resulted in increased adhesion of NK cells and susceptibility to NK cell-mediated cytolysis compared with control transfection. Moreover, both enhanced adhesion and susceptibility of fractalkine-transfected cells were markedly suppressed by soluble fractalkine or anti-CX3CR1 Ab. Our results suggest that fractalkine plays an important role not only in the binding of NK cells to endothelial cells, but also in NK cell-mediated endothelium damage, which may result in vascular injury. (+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:
3. Heart disease
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.
Disease progression can be classified into several types based on the pattern of worsening:
1. Chronic progressive disease: In this type, the disease worsens steadily over time, with a gradual increase in symptoms and decline in function. Examples include rheumatoid arthritis, osteoarthritis, and Parkinson's disease.
2. Acute progressive disease: This type of disease worsens rapidly over a short period, often followed by periods of stability. Examples include sepsis, acute myocardial infarction (heart attack), and stroke.
3. Cyclical disease: In this type, the disease follows a cycle of worsening and improvement, with periodic exacerbations and remissions. Examples include multiple sclerosis, lupus, and rheumatoid arthritis.
4. Recurrent disease: This type is characterized by episodes of worsening followed by periods of recovery. Examples include migraine headaches, asthma, and appendicitis.
5. Catastrophic disease: In this type, the disease progresses rapidly and unpredictably, with a poor prognosis. Examples include cancer, AIDS, and organ failure.
Disease progression can be influenced by various factors, including:
1. Genetics: Some diseases are inherited and may have a predetermined course of progression.
2. Lifestyle: Factors such as smoking, lack of exercise, and poor diet can contribute to disease progression.
3. Environmental factors: Exposure to toxins, allergens, and other environmental stressors can influence disease progression.
4. Medical treatment: The effectiveness of medical treatment can impact disease progression, either by slowing or halting the disease process or by causing unintended side effects.
5. Co-morbidities: The presence of multiple diseases or conditions can interact and affect each other's progression.
Understanding the type and factors influencing disease progression is essential for developing effective treatment plans and improving patient outcomes.
The disease begins with endothelial dysfunction, which allows lipid accumulation in the artery wall. Macrophages take up oxidized lipids and become foam cells, which die and release their contents, including inflammatory cytokines, leading to further inflammation and recruitment of more immune cells.
The atherosclerotic plaque can rupture or ulcerate, leading to the formation of a thrombus that can occlude the blood vessel, causing ischemia or infarction of downstream tissues. This can lead to various cardiovascular diseases such as myocardial infarction (heart attack), stroke, and peripheral artery disease.
Atherosclerosis is a multifactorial disease that is influenced by genetic and environmental factors such as smoking, hypertension, diabetes, high cholesterol levels, and obesity. It is diagnosed by imaging techniques such as angiography, ultrasound, or computed tomography (CT) scans.
Treatment options for atherosclerosis include lifestyle modifications such as smoking cessation, dietary changes, and exercise, as well as medications such as statins, beta blockers, and angiotensin-converting enzyme (ACE) inhibitors. In severe cases, surgical interventions such as bypass surgery or angioplasty may be necessary.
In conclusion, atherosclerosis is a complex and multifactorial disease that affects the arteries and can lead to various cardiovascular diseases. Early detection and treatment can help prevent or slow down its progression, reducing the risk of complications and improving patient outcomes.
Role of microglia in disease
Respiratory syncytial virus
List of MeSH codes (D12.776)
List of MeSH codes (D23)
Outline of immunology
List of MeSH codes (D12.644)
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Don't Say No
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We, Too, Have a Job to Do
2021 Akkar explosion
Leina, Saare County
CX3CR1-fractalkine axis drives kinetic changes of monocytes in fibrotic interstitial lung diseases
DeCS - Termos Novos
Human Cytokines, Growth Factors & Chemokines from RDI
Blood coagulation protein fibrinogen promotes autoimmunity and demyelination via chemokine release and antigen presentation -...
Endogenous glucocorticoids prevent gastric metaplasia by suppressing spontaneous inflammation - PubMed
Philip Murphy, M.D. | NIH: National Institute of Allergy and Infectious Diseases
Proposal for Human Respiratory Syncytial Virus Nomenclature below the Species Level - Volume 27, Number 6-June 2021 - Emerging...
Division of Oncology - Research output - Research Profiles at Washington University School of Medicine
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Pharos : Target Details - CX3CR1
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Cytokines: Made Simple for the Ophthalmologists
CX3CL1, a chemokine finely tuned to adhesion: critical roles of the stalk glycosylation and the membrane domain | Biology Open ...
NDF-RT Code NDF-RT Name
Other Peptide Receptors
Anti-CXCL9: Rabbit CXCL9 Antibody | sputnic-group.ru : Cell Applications
Philip M. Murphy, A.B., M.D. | Principal Investigators | NIH Intramural Research Program
NEW (2008) MESH HEADINGS WITH SCOPE NOTES (UNIT RECORD FORMAT; 11/05/2007
The role of immune system in the development of periodontal disease: a brief review
- Deficiency of various chemokines, chemokine receptors and leukocyte adhesion molecules that are known to participate in mononuclear leukocyte emigration, such as monocyte chemoattractant protein-1 and its receptor chemokine (CC motif) receptor 2, CX3C chemokine receptor 1 and vascular cell adhesion molecule 1, results in decreased formation of atherosclerotic lesions. (nih.gov)
- CX3CR1 is a G-protein-coupled seven-transmembrane chemokine receptor, also called GPR13 or V28. (biolegend.com)
- Due to continuous recycling of many chemokine receptors, it may be worthwhile to consider staining at room temperature or at 37°C if the staining at lower temperature (which can potentially reduce receptor turnover) is not optimal. (biolegend.com)
- They represent an exception among chemokines in that they specifically interact with a single type of receptor, named CXCR3. (sputnic-group.ru)
- Reporter cells were transfected with either the expression plasmid for mouse chemokine (C-C motif) receptor 10 (Ccr10) or the mock plasmid and treated with various concentrations of the reference agonist. (tansobio.com)
- Most chemokine receptors are able to bind multiple high-affinity chemokine ligands, but the ligands for a given receptor are almost always restricted to the same structural subclass. (tansobio.com)
- Most chemokines bind to more than one receptor subtype. (tansobio.com)
- The tables include both standard chemokine receptor names  and aliases. (tansobio.com)
- An atypical addition to the chemokine receptor nomenclature: IUPHAR Review 15. (tansobio.com)
- This was not due to detectable APOE-specific differences in expression of microglial major histocompatibility complex class II, C-C chemokine receptor (CCR) type 1, CCR2, CX3C chemokine receptor 1 (CX3CR1), or C5a anaphylatoxin chemotactic receptor (C5aR). (nih.gov)
- T280M variation of the CX3C receptor gene is associated with increased risk for severe respiratory syncytial virus bronchiolitis. (cdc.gov)
- Associations of chemokine receptor polymorphisms With HIV-1 mother-to-child transmission in sub-Saharan Africa: possible modulation of genetic effects by antiretrovirals. (cdc.gov)
- Sequence variants of chemokine receptor genes and susceptibility to HIV-1 infection. (cdc.gov)
- Association of chemokine receptor gene variants with HIV-1 genotype predicted tropism. (cdc.gov)
- Chemotaxis elicited by Recombinant Human CX3CL1/Fractalkine (100 ng/mL) is neutralized (green line) by increasing concentrations of Mouse Anti-Human CX3CL1/Fractalkine Chemokine Domain Monoclonal Antibody (Catalog # MAB3652). (rndsystems.com)
- CX3CL1, also known as Fractalkine, is a type I membrane protein in which a chemokine domain possessing a unique C-X3-C cysteine motif is tethered on a long mucin-like stalk. (rndsystems.com)
- CX3CL1 is a unique transmembrane molecule with a CX3C-motif chemokine domain and a mucin-like stalk. (biolegend.com)
- For example, insights may be gained to distinguish the contribution of chemokines, chemokine receptors and adhesion molecules to the recruitment, survival or proliferation of different leukocyte types in atherosclerotic lesions. (nih.gov)
- Does staining at room temperature or even at 37°C help for checking chemokine receptors expression? (biolegend.com)
- These include a large family of chemokine receptors and a smaller group of classical chemoattractant receptors, which together differentially regulate specific leukocyte trafficking in support of innate and adaptive immune responses. (nih.gov)
- Chemokine receptors comprise a large subfamily of 7TM proteins that bind one or more chemokines, a large family of small cytokines typically possessing chemotactic activity for leukocytes. (tansobio.com)
- Chemokine receptors can be divided by function into two main groups: G protein-coupled chemokine receptors, which mediate leukocyte trafficking, and "Atypical chemokine receptors", which may signal through non-G protein-coupled mechanisms and act as chemokine scavengers to downregulate inflammation or shape chemokine gradients . (tansobio.com)
- Receptors for inflammatory chemokines are typically highly promiscuous with regard to ligand specificity, and may lack a selective endogenous ligand. (tansobio.com)
- G protein-coupled chemokine receptors are named acccording to the class of chemokines bound, whereas ACKR is the root acronym for atypical chemokine receptors . (tansobio.com)
- There can be substantial cross-species differences in the sequences of both chemokines and chemokine receptors, and in the pharmacology and biology of chemokine receptors. (tansobio.com)
- Endogenous and microbial non-chemokine ligands have also been identified for chemokine receptors. (tansobio.com)
- Many chemokine receptors function as HIV co-receptors, but CCR5 is the only one demonstrated to play an essential role in HIV/AIDS pathogenesis. (tansobio.com)
- Update on the extended family of chemokine receptors and introducing a new nomenclature for atypical chemokine receptors. (tansobio.com)
- The integration of pathogen-associated molecular patterns (PAMPs) from microorganisms with their surface receptors in the immune cells, induces the production of several cytokines and chemokines that presents either a pro- and/or anti-inflammatory role by stimulating the secretion of a great variety of antibody subtypes and the activation of mechanisms of controlling the disease, such as the regulatory T cells. (bvsalud.org)
- shift interactions are composed into micelle-like acids, CXC contraction receptors, CC composition receptors, CX3C cleavage nucleosides and 1292dupG system associates that have to the 4 human regions of channels they have. (erik-mill.de)
- 1 Although CXC chemokines with an N-terminal ELR (Glu-Leu-Arg) motif, such as IL-8, are specific chemoattractants for neutrophils, those lacking the N-terminal ELR motif, such as monokine induced by interferon- (IFN ) (CXCL9/Mig), CXCL10/IP-10, and IFN -inducible T-cell -chemoattractant (CXCL11/I-TAC), do not act as chemoattractants for neutrophils, but attract T helper (Th) 1 cells. (sputnic-group.ru)
- Monokines induced by interferon-gamma/Chemokine (C-X-C motif) ligand 9 (MIG/CXCL9), thymus and activation-regulated chemokine/Chemokine (C-C motif) ligand 17 (TARC/CCL17) are chemotactic factors that specifically collect and activate leukocytes, which are considered as chemoattractants of T helper cells. (biomedcentral.com)
- However, little is known in KD patients about the chemotactic factors of T helper type-1 cells (Th1) and T helper type-2 cells (Th2), plasma monokines induced by interferon-gamma/Chemokine (C-X-C motif) ligand 9 (MIG/CXCL9) and thymus and activation-regulated chemokine/Chemokine (C-C motif) ligand 17 (TARC/CCL17). (biomedcentral.com)
- 7. Retinoic acid-inducible gene-I is induced by double-stranded RNA and regulates the expression of CC chemokine ligand (CCL) 5 in human mesangial cells. (nih.gov)
- CX3C chemokines are chemotactic for natural killer cells, monocytes, and activated T-cells. (nih.gov)
- BACKGROUND The chemoattractant cytokines (chemokines) are ubiquitous chemotactic molecules that play major roles in acute and chronic inflammatory conditions. (sputnic-group.ru)
- These CXCR3-agonistic chemokines play an important role in inflammation through their T-cell chemotactic and adhesion-promoting activities. (sputnic-group.ru)
Cytokines and chemokines1
- 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)
- An assumption is often made that leukocyte recruitment is diminished if a reduction in lesions is found in chemokine- or adhesion molecule-deficient animals. (nih.gov)
- The CXC chemokine family is a pleiotropic family of molecules that are involved in the trafficking of various leukocyte subsets, angiogenesis, and vascular remodeling. (sputnic-group.ru)
- These interferon-gamma inducible chemokines (CXCL9/Mig, CXCL10/IP-10, CXCL11/I-TAC) belong to the CXC sub-family. (sputnic-group.ru)
- Fractalkine is a transmembrane protein and chemokine involved in the adhesion and migration of leukocytes. (nih.gov)
- Group of chemokines with the first two cysteines separated by three amino acids. (nih.gov)
- They are divided into 4 families defined by the number of amino acids between the N-terminal cysteine residues (CC, CXC, CCX, and CX3C). (sputnic-group.ru)
- n = 17) and CX3C ( n = 1) chemokines all have four conserved cysteines, with zero, one and three amino acids separating the first two cysteines respectively. (tansobio.com)
- 11. Melanoma differentiation-associated gene 5 regulates the expression of a chemokine CXCL10 in human mesangial cells: implications for chronic inflammatory renal diseases. (nih.gov)
- These examples provide evidence that the chemokines, CXCL9 and CXCL10, attract T cells to the site of infection and may provide in some cases, optimal defense against microbial pathogens. (sputnic-group.ru)
- 2 CXCL9 is highly expressed in skin lichen planus compared with other chemokines, such as CCL2, CCL20, and CXCL8. (sputnic-group.ru)
- ... [read more] non-hematopoietic roles have been identified for many chemokines in the areas of embryonic development, immune cell proliferation, activation and death, viral infection, and as antibiotics, among others. (tansobio.com)
- For instance, interleukin 8 (IL-8) is also considered a pro-inflammatory chemokine and is often designated as CXCL8. (eophtha.com)
- Zlotnik A, Yoshie O. Chemokines: a new classification system and their role in immunity. (tansobio.com)
- Dr. Murphy's research interests include immunoregulation by chemokines and related chemoattractants. (nih.gov)
- 11. Expression cloning of the STRL33/BONZO/TYMSTRligand reveals elements of CC, CXC, and CX3C chemokines. (nih.gov)
- The name and number of human members in each class of chemokines are on the right. (nih.gov)