Chemokine CCL27
Chemokine CCL21
Chemokine CCL22
Chemokine CCL17
Chemokine CCL2
Chemokine CCL19
Chemokine CCL5
Chemokine CCL20
Chemokine CCL1
Chemokines, CC
Receptors, Chemokine
Chemokine CCL3
Chemokine CCL7
Chemokines
Receptors, CCR10
Chemokine CCL4
Chemokine CXCL12
Receptors, CCR1
Chemokine CXCL10
Chemokine CCL8
Receptors, CCR2
Chemokine CCL11
Chemokine CCL24
Receptors, CCR7
Receptors, CCR8
Chemokine CXCL1
Chemotaxis, Leukocyte
Receptors, CCR4
Chemokines, CXC
Chemokine CX3CL1
Macrophage Inflammatory Proteins
Receptors, CCR5
Receptors, CCR3
Cell Movement
Chemokine CXCL2
Chemokine CXCL13
Receptors, CXCR4
Chemokine CXCL11
Chemotaxis
Chemokine CXCL6
Cells, Cultured
Dendritic Cells
Chemokine CXCL5
Cytokines
Mice, Knockout
Receptors, CXCR3
Monocytes
Macrophages
Gene Expression Regulation
RNA, Messenger
T-Lymphocytes
Inflammation
Reverse Transcriptase Polymerase Chain Reaction
Enzyme-Linked Immunosorbent Assay
Flow Cytometry
Receptors, Interleukin-8B
Signal Transduction
Dermatitis, Atopic
Up-Regulation
Monocyte Chemoattractant Proteins
Disease Models, Animal
Skin
Mice, Transgenic
Interleukin-8
Ligands
Receptors, CCR6
CD4-Positive T-Lymphocytes
Receptors, Interleukin-8A
Lymph Nodes
NF-kappa B
Carbon Tetrachloride
Immunohistochemistry
Receptors, Cytokine
T-Lymphocytes, Regulatory
Tumor Necrosis Factor-alpha
Chemokines, CX3C
Receptors, CXCR5
Protein Binding
Chemotactic Factors
CD8-Positive T-Lymphocytes
Endothelial Cells
Lymphocyte Activation
Monokines
Receptors, HIV
Duffy Blood-Group System
Chemotactic Factors, Eosinophil
Neutrophil Infiltration
Neutrophils
Heterocyclic Compounds
Lung
Leukocytes
Gene Expression
Inflammation Mediators
Interferon-gamma
Th2 Cells
Cell Migration Inhibition
HIV-1
Molecular Sequence Data
Eosinophils
Intercellular Signaling Peptides and Proteins
Lipopolysaccharides
Down-Regulation
Amino Acid Sequence
Epithelial Cells
Leukocytes, Mononuclear
Th1 Cells
Lymphoid Tissue
T-Lymphocyte Subsets
Gene Expression Profiling
Platelet Factor 4
Stromal Cells
Immunity, Innate
Bronchoalveolar Lavage Fluid
Transfection
Drug-Induced Liver Injury
Endothelium, Lymphatic
RFLAT-1: a new zinc finger transcription factor that activates RANTES gene expression in T lymphocytes. (1/1514)
RANTES (Regulated upon Activation, Normal T cell Expressed and Secreted) is a chemoattractant cytokine (chemokine) important in the generation of inflammatory infiltrate and human immunodeficiency virus entry into immune cells. RANTES is expressed late (3-5 days) after activation in T lymphocytes. Using expression cloning, we identified the first "late" T lymphocyte associated transcription factor and named it "RANTES Factor of Late Activated T Lymphocytes-1" (RFLAT-1). RFLAT-1 is a novel, phosphorylated, zinc finger transcription factor that is expressed in T cells 3 days after activation, coincident with RANTES expression. While Rel proteins play the dominant role in RANTES gene expression in fibroblasts, RFLAT-1 is a strong transactivator for RANTES in T cells. (+info)Similarities and differences in RANTES- and (AOP)-RANTES-triggered signals: implications for chemotaxis. (2/1514)
Chemokines are a family of proinflammatory cytokines that attract and activate specific types of leukocytes. Chemokines mediate their effects via interaction with seven transmembrane G protein-coupled receptors (GPCR). Using CCR5-transfected HEK-293 cells, we show that both the CCR5 ligand, RANTES, as well as its derivative, aminooxypentane (AOP)- RANTES, trigger immediate responses such as Ca2+ influx, receptor dimerization, tyrosine phosphorylation, and Galphai as well as JAK/STAT association to the receptor. In contrast to RANTES, (AOP)-RANTES is unable to trigger late responses, as measured by the association of focal adhesion kinase (FAK) to the chemokine receptor complex, impaired cell polarization required for migration, or chemotaxis. The results are discussed in the context of the dissociation of the late signals, provoked by the chemokines required for cell migration, from early signals. (+info)Induction of macrophage C-C chemokine expression by titanium alloy and bone cement particles. (3/1514)
Particulate wear debris is associated with periprosthetic inflammation and loosening in total joint arthroplasty. We tested the effects of titanium alloy (Ti-alloy) and PMMA particles on monocyte/macrophage expression of the C-C chemokines, monocyte chemoattractant protein-1 (MCP-1), monocyte inflammatory protein-1 alpha (MIP-1alpha), and regulated upon activation normal T expressed and secreted protein (RANTES). Periprosthetic granulomatous tissue was analysed for expression of macrophage chemokines by immunohistochemistry. Chemokine expression in human monocytes/macrophages exposed to Ti-alloy and PMMA particles in vitro was determined by RT-PCR, ELISA and monocyte migration. We observed MCP-1 and MIP-1alpha expression in all tissue samples from failed arthroplasties. Ti-alloy and PMMA particles increased expression of MCP-1 and MIP-1alpha in macrophages in vitro in a dose- and time-dependent manner whereas RANTES was not detected. mRNA signal levels for MCP-1 and MIP-1alpha were also observed in cells after exposure to particles. Monocyte migration was stimulated by culture medium collected from macrophages exposed to Ti-alloy and PMMA particles. Antibodies to MCP-1 and MIP-1alpha inhibited chemotactic activity of the culture medium samples. Release of C-C chemokines by macrophages in response to wear particles may contribute to chronic inflammation at the bone-implant interface in total joint arthroplasty. (+info)RANTES, IFN-gamma, CCR1, and CCR5 mRNA expression in peripheral blood, lymph node, and bronchoalveolar lavage mononuclear cells during primary simian immunodeficiency virus infection of macaques. (4/1514)
Primary infection of macaques with pathogenic isolates of simian immunodeficiency virus (SIV) (as a model of HIV infection in humans) represents a unique opportunity to study early lentivirus/host interactions. We sought to determine whether there is a temporal relationship linking SIV replication and dissemination and the expression of the chemokine RANTES (regulated upon activation normal T cell expressed and secreted) and the SIV/HIV coreceptor CCR5 in different tissues during acute SIV infection of macaques. Four cynomolgus macaques were inoculated intravenously with a pathogenic primary isolate of SIVmac251. RT-PCR was used to monitor the expression of RANTES and CCR5 mRNA in fresh isolated mononuclear cells from blood, lymph node, and bronchoalveolar lavages. These expressions were compared to those of IFN-gamma as an indicator of the development of the immune response and to another receptor for RANTES, CCR1, which is not described as a coreceptor for SIV/HIV-1 entry. An enhancement of CCR1/CCR5 mRNA expression was noticed during primary SIVmac251 infection of macaques, mainly in tissue. In the three different compartments investigated, IFN-gamma and RANTES overexpression was noticed by the time of systemic viral replication containment. Our results put CCR5 and RANTES mRNA expression back in the context of inflammatory and immune responses to SIV primary infection. (+info)Chemokine expression in CF epithelia: implications for the role of CFTR in RANTES expression. (5/1514)
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)IL-15 induces the expression of chemokines and their receptors in T lymphocytes. (6/1514)
IL-15 is a T cell growth factor that shares many biological activities with IL-2 and uses the same beta/gamma polypeptides of the IL-2R complex for signal transduction. Accumulating evidence implicates an important role for this cytokine in the inflammatory response of the host. Consistent with such a role, IL-15 has been shown to be a chemoattractant for T lymphocytes, NK cells, and neutrophils. Extending these observations, we now show that IL-15 is a potent inducer of CC-, CXC-, and C-type chemokines in T lymphocytes. In addition, we demonstrate that IL-15 induces CC chemokine receptors, but not CXC chemokine receptors, in a dose-dependent manner. Thus, our findings suggest that the proinflammatory effects of IL-15 at least in part may be due to the induction of chemokines and their receptors in T cells. Furthermore, we demonstrate that IL-15 promotes entry and replication of macrophage-tropic HIV in T lymphocytes and suggest a plausible mechanism by which IL-15, a cytokine that is elevated in HIV-infected individuals, may promote the transition of HIV displaying the M-tropic phenotype primarily associated with the initial transmission into the T cell-tropic phenotype that predominates as the disease progresses. (+info)IL-12 gene as a DNA vaccine adjuvant in a herpes mouse model: IL-12 enhances Th1-type CD4+ T cell-mediated protective immunity against herpes simplex virus-2 challenge. (7/1514)
IL-12 has been shown to enhance cellular immunity in vitro and in vivo. Recent reports have suggested that combining DNA vaccine approach with immune stimulatory molecules delivered as genes may significantly enhance Ag-specific immune responses in vivo. In particular, IL-12 molecules could constitute an important addition to a herpes vaccine by amplifying specific immune responses. Here we investigate the utility of IL-12 cDNA as an adjuvant for a herpes simplex virus-2 (HSV-2) DNA vaccine in a mouse challenge model. Direct i.m. injection of IL-12 cDNA induced activation of resting immune cells in vivo. Furthermore, coinjection with IL-12 cDNA and gD DNA vaccine inhibited both systemic gD-specific Ab and local Ab levels compared with gD plasmid vaccination alone. In contrast, Th cell proliferative responses and secretion of cytokines (IL-2 and IFN-gamma) and chemokines (RANTES and macrophage inflammatory protein-1alpha) were significantly increased by IL-12 coinjection. However, the production of cytokines (IL-4 and IL-10) and chemokine (MCP-1) was inhibited by IL-12 coinjection. IL-12 coinjection with a gD DNA vaccine showed significantly better protection from lethal HSV-2 challenge compared with gD DNA vaccination alone in both inbred and outbred mice. This enhanced protection appears to be mediated by CD4+ T cells, as determined by in vivo CD4+ T cell deletion. Thus, IL-12 cDNA as a DNA vaccine adjuvant drives Ag-specific Th1 type CD4+ T cell responses that result in reduced HSV-2-derived morbidity as well as mortality. (+info)Requirements for measles virus induction of RANTES chemokine in human astrocytoma-derived U373 cells. (8/1514)
Interferons and chemokines play a critical role in regulating the host response to viral infection. Measles virus, a member of the Paramyxoviridae family, induces RANTES expression by astrocytes. We have examined the mechanism of this induction in U373 cells derived from a human astrocytoma. RANTES was induced in a dose- and time-dependent manner by measles virus infection. Inhibition of receptor binding by the anti-CD46 antibody TRA-2.10 and of virus-membrane fusion by the tripeptide X-Phe-Phe-Gly reduced RANTES expression. Formalin-inactivated virus, which can bind but not fuse, and extensively UV-irradiated virus, which can bind and fuse, were both ineffective. Therefore, virus binding to the cellular receptor CD46 and subsequent membrane fusion were necessary, but not sufficient, to induce RANTES. UV irradiation of virus for less than 10 min proportionally inhibited viral transcription and RANTES expression. RANTES induction was decreased in infected cells treated with ribavirin, which inhibits measles virus transcription. However, RANTES mRNA was superinduced by measles virus in the presence of cycloheximide. These data suggest that partial transcription of the viral genome is sufficient and necessary for RANTES induction, whereas viral protein synthesis and replication are not required. This hypothesis was supported by the fact that RANTES was induced through transient expression of the measles virus nucleocapsid gene but not by measles genes encoding P or L proteins or by leader RNA in A549 cells. Thus, transcription of specific portions of measles virus RNA, such as the nucleocapsid gene, appears able to generate the specific signaling required to induce RANTES gene expression. (+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.
Also known as eczema or atopic eczema.
Dermatitis, Atopic is a common condition that affects people of all ages but is most prevalent in children. It is often associated with other atopic conditions such as asthma and allergies. The exact cause of dermatitis, atopic is not known, but it is thought to involve a combination of genetic and environmental factors.
Symptoms of Dermatitis, Atopic:
* Redness and dryness of the skin
* Scaling and flaking of the skin
* Itching and burning sensations
* Thickening and pigmentation of the skin
* Small blisters or weeping sores
Atopic dermatitis can occur anywhere on the body but is most commonly found on the face, neck, hands, and feet.
Treatment for Dermatitis, Atopic:
* Moisturizers to keep the skin hydrated and reduce dryness
* Topical corticosteroids to reduce inflammation
* Antihistamines to relieve itching
* Phototherapy with ultraviolet light
* Oral immunomodulators for severe cases
It is important to note that dermatitis, atopic is a chronic condition, and treatment should be ongoing. Flare-ups may occur, and adjustments to the treatment plan may be necessary.
Prevention of Dermatitis, Atopic:
* Avoiding triggers such as soaps, detergents, and stress
* Keeping the skin well-moisturized
* Avoiding extreme temperatures and humidity
* Wearing soft, breathable clothing
* Using mild cleansers and avoiding harsh chemicals
Early diagnosis and treatment of dermatitis, atopic can help improve the quality of life for those affected. It is important to work with a healthcare professional to develop an appropriate treatment plan and manage symptoms effectively.
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.
The symptoms of carbon tetrachloride poisoning can vary depending on the level and duration of exposure, but may include:
* Respiratory problems, such as coughing, wheezing, and shortness of breath
* Nausea and vomiting
* Abdominal pain and diarrhea
* Headaches and dizziness
* Confusion and disorientation
* Slurred speech and loss of coordination
* Seizures and coma
If you suspect that you or someone else has been exposed to carbon tetrachloride, it is essential to seek medical attention immediately. Treatment for carbon tetrachloride poisoning typically involves supportive care, such as oxygen therapy and hydration, as well as medications to manage symptoms and remove the toxin from the body. In severe cases, hospitalization may be necessary.
Prevention is key when it comes to carbon tetrachloride poisoning. If you work with or are exposed to CTC, it is important to take safety precautions such as wearing protective clothing and equipment, using proper ventilation, and following all safety protocols. It is also essential to handle the chemical with care and store it in a safe location.
In conclusion, carbon tetrachloride poisoning can be a serious and potentially deadly condition that requires immediate medical attention. If you suspect exposure to CTC, it is crucial to seek medical help right away. By taking safety precautions and being aware of the risks associated with this chemical, you can prevent carbon tetrachloride poisoning and protect your health.
The definition of DILI has been revised several times over the years, but the most recent definition was published in 2013 by the International Consortium for DILI Research (ICDCR). According to this definition, DILI is defined as:
"A clinically significant alteration in liver function that is caused by a medication or other exogenous substance, and is not related to underlying liver disease. The alteration may be biochemical, morphological, or both, and may be acute or chronic."
The ICDCR definition includes several key features of DILI, including:
1. Clinically significant alteration in liver function: This means that the liver damage must be severe enough to cause symptoms or signs of liver dysfunction, such as jaundice, nausea, vomiting, or abdominal pain.
2. Caused by a medication or other exogenous substance: DILI is triggered by exposure to certain drugs or substances that are not related to underlying liver disease.
3. Not related to underlying liver disease: This means that the liver damage must not be caused by an underlying condition such as hepatitis B or C, alcoholic liver disease, or other genetic or metabolic disorders.
4. May be acute or chronic: DILI can occur as a sudden and severe injury (acute DILI) or as a slower and more insidious process (chronic DILI).
The ICDCR definition provides a standardized way of defining and diagnosing DILI, which is important for clinicians and researchers to better understand the cause of liver damage in patients who are taking medications. It also helps to identify the drugs or substances that are most likely to cause liver injury and to develop strategies for preventing or treating DILI.
CCL5
Chemokine
Foam cell
CC chemokine receptors
CCR5
CCR3 (gene)
Tumor microenvironment
Evasin
GPR75
Specialized pro-resolving mediators
CCR1
Photoaging
Eosinophil
Immunologic Constant of Rejection
CCR4
NR58-3.14.3
Major histocompatibility complex, class I-related
Index of immunology articles
Alan M. Krensky
Chromosome 17
Duffy antigen system
Role of microglia in disease
KLF13
CCR5 receptor antagonist
Murine respirovirus
Megakaryocyte
E-selectin
2014 Ju-Jitsu World Championships
Bolley Johnson
Don't Say No
Oligomeric Structure of the Chemokine CCL5/RANTES from NMR, MS, and SAXS Data - Arizona State University
Chemokine CCL5 | Profiles RNS
Chemokine CCL5 - McMaster Experts
DeCS 2008 - Changed terms
Intratumoral γδ T-Cell Infiltrates, Chemokine (C-C Motif) Ligand 4/Chemokine (C-C Motif) Ligand 5 Protein Expression and...
Autoantibodies as Diagnostic Markers and Mediator of Joint Inflammation in Arthritis
Publication Detail
CCL5
- Early...
MeSH Browser
Human Parainfluenza Viruses (HPIV) and Other Parainfluenza Viruses: Background, Pathophysiology, Etiology
Frontiers | Systems Biomedicine of Rabies Delineates the Affected Signaling Pathways
Rhinovirus (RV) Infection (Common Cold) Clinical Presentation: History, Physical Examination, Complications
Human Parainfluenza Viruses (HPIV) and Other Parainfluenza Viruses: Background, Pathophysiology, Etiology
Sequential actions of EOMES and T-BET promote stepwise maturation of natural killer cells | Nature Communications
MicroRNA-Mediated Calcineurin Signaling Activation Induces CCL2, CCL3, CCL5, IL8 and Chemotactic Activities in 4,4'-Methylene...
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NIOSHTIC-2 Search Results - Full View
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DeCS
MeSH Browser
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Single-cell analysis of the aged ovarian immune system reveals a shift towards adaptive immunity and attenuated cell function |...
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Ligand2
- C-C motif chemokine ligand 2 [Sour. (gsea-msigdb.org)
- The C-C chemokine receptor types 2 and 5 (CCR2 and CCR5), and their respective ligands, C-C chemokine ligand types 2 (CCL2/MCP-1) and 5 (CCL5/RANTES) play an important role in polarizing monocytes to M1 macrophages [ 12 ]. (biomedcentral.com)
Motif1
- It functions as one of the natural ligands for the chemokine receptor chemokine (C-C motif) receptor 5 (CCR5), and it suppresses in vitro replication of the R5 strains of HIV-1, which use CCR5 as a coreceptor. (nih.gov)
Cytokines and chemokines2
- Human Qbeads Inflammation Panel Kit allows the measurement of seven human cytokines and chemokines from either serum or in vitro samples. (sartorius.com)
- In animal models of acute allergic inflammation, cytokines and chemokines such as IL-4, IL-5, IL-9, IL-13, CCL5 and CCL11 have been shown to induce eosinophilic airway inflammation, antigen-specific IgE production, and airway hyperresponsiveness. (ristorante-da-luciano.de)
Proteins1
- Chemokines form a superfamily of secreted proteins involved in immunoregulatory and inflammatory processes. (nih.gov)
Cytokine2
- Additionally, M2 related cytokine/chemokine receptors IL-4R and CCR1 were significantly dysregulated in IL-6KO BKC treated mice. (cdc.gov)
- We analyze the effect of aging on gene expression and chemokine and cytokine networks and show an overall decreased expression of inflammatory mediators together with an increased expression of senescent cells recognition receptors. (elifesciences.org)
CCL32
- Multiplex protein analysis showed expression of multiple M1-related cytokines such IFN-g, CCL3, CCL4, CCL5, and CCL7 significantly modulated in IL6-KO BKC treated mice compared to C57. (cdc.gov)
- In a study, the liver granulomas of chronically infected mice showed more cells and greater collagen deposition which was associated with higher levels of IL-5, IL-13, CCL3 and CCL5. (ristorante-da-luciano.de)
RECEPTORS2
- May activate several chemokine receptors including CCR1, CCR3, CCR4 and CCR5. (nih.gov)
- A CC-type chemokine with specificity for CCR7 RECEPTORS. (bvsalud.org)
Mediators3
- Interplay between several molecules (cytokines, chemokines, proteases, and inflammatory mediators) culminates in causing damage to the articular cartilage and bones. (hindawi.com)
- Upon encountering outside stimuli, alveolar macrophages react by phagocytosis as well as producing and secreting different mediators such as cytokines, chemokines, and others, into the alveoli microenvironment to orchestrate the initiation of inflammatory/immune responses. (cdc.gov)
- Those include interferons (IFNs), essential for the antiviral response proinflammatory mediators, and chemokines. (ristorante-da-luciano.de)
Protein1
- The chemokine with chemotactic activity CCL5 is a 7.8 kDa protein and was discovered in activated T cells. (ristorante-da-luciano.de)
CCL211
- The model he proposed was that 1) DC enters lymphatics thanks to a chemokine gradient (including CCL21 and CX3CL1) and 2) they synthesize a surface hyaluronan glycocalyx that acts as adhesin. (cfcd.fr)
Inflammatory1
- The cytokines/chemokines included are implicated in inflammatory responses to disease states including autoimmune diseases, chronic inflammation, and infections, including viral infections such as COVID-19. (sartorius.com)
Descriptor1
- Chemokine CCL5" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (wakehealth.edu)
Macrophages2
- CCL5 is now known to be secreted by many other cell types, including macrophages, endothelial cells, tumor cells, smooth muscle cells, platelets, and hepatic stellate cells. (ristorante-da-luciano.de)
- The expression of CCL5 is detected in atherosclerotic plaques and in monocyte/macrophages. (ristorante-da-luciano.de)
Genes2
MONOCYTES1
- This chemokine, a member of the CC subfamily, functions as a chemoattractant for blood monocytes, memory T helper cells and eosinophils. (nih.gov)
Expression3
- In addition, our western blotting study further revealed that the GLE treatment caused an increase in expression of CCL5 chemokine in the cultured B-lymphocytes. (nih.gov)
- There are many epidemiological and clinical studies in several human diseases demonstrating the expression of CCL5 and correlation with indices of disease activity. (ristorante-da-luciano.de)
- EGFR, HER2) on melanoma cells, and(b) CL-11-dependent promotion of immunosuppressive TME, characterized by a high proportion of myeloid cells and a low proportion of lymphocytes, lack of cytotoxic T cell infiltrating in the tumor core, increased angiogenesis, low levels of intratumor expression of cytokines/chemokines with antitumor properties (e.g. (bioz.com)
Human2
- 4. Chemokine CCL5 immune subtypes of human liver cancer with prognostic significance. (nih.gov)
- Recombinant Human C-C chemokine receptor type 8(CCR8) referenced in "The chemokine CCL1 triggers an AMFR-SPRY1 pathway that promotes differentiation of lung fibroblasts into myofibroblasts and drives pulmonary fibrosis", Immunity , 2021. (cusabio.com)
Increase1
- This increase of hepatic CCL5 could mediate leukocyte recruitment to the organ and contribute to the systemic inflammation. (ristorante-da-luciano.de)
Play1
- CCL5 is associated with chronic inflammation and may play a direct role in angiogenesis and in other angiogenesis-dependent processes, such as the progression of some tumors. (ristorante-da-luciano.de)
Publications2
- 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)
Production1
- The production of CCL5 has been observed in most viral infections of the respiratory tract. (ristorante-da-luciano.de)
RANTES3
- 24. Expression of CCR5 receptors on Reed-Sternberg cells and Hodgkin lymphoma cell lines: involvement of CCL5/Rantes in tumor cell growth and microenvironmental interactions. (nih.gov)
- 38. Role of myeloid-derived chemokine CCL5/RANTES at an early stage of atherosclerosis. (nih.gov)
- Elevated serum RANTES chemokine levels in autoimmune Addison disease. (cdc.gov)
CCL22
- Calcineurin inhibitor tacrolimus (FK506) attenuated the MDI-GSH conjugate-mediated induction of CCL2, CCL3, CCL5, and CXCL8/IL8 but not others. (cdc.gov)
- Transfection of either miR-inhibitor-206-3p or miR-inhibitor-381-3p in macrophages induced chemokine CCL2, CCL3, CCL5, and CXCL8 transcription, whereas FK506 attenuated the miR-inhibitor-206-3p or miR-inhibitor-381-3p-mediated effects. (cdc.gov)
Motif2
- 32. Chemokine C-C motif receptor 5 and C-C motif ligand 5 promote cancer cell migration under hypoxia. (nih.gov)
- It functions as one of the natural ligands for the chemokine receptor chemokine (C-C motif) receptor 5 (CCR5), and it suppresses in vitro replication of the R5 strains of HIV-1, which use CCR5 as a coreceptor. (nih.gov)
Several chemokine2
Receptors1
- The discussed chemokines in this review, their synonyms, receptors, activities and sources were summarized in Table 4 . (medscape.com)
CCR56
- 22. Role of CCL5 in invasion, proliferation and proportion of CD44+/CD24- phenotype of MCF-7 cells and correlation of CCL5 and CCR5 expression with breast cancer progression. (nih.gov)
- 23. Genetic variants in CCL5 and CCR5 genes and serum VEGF-A levels predict efficacy of bevacizumab in metastatic colorectal cancer patients. (nih.gov)
- 26. Role of CCL5 and CCR5 gene polymorphisms in epidermal growth factor receptor signalling blockade in metastatic colorectal cancer: analysis of the FIRE-3 trial. (nih.gov)
- 29. The Diagnostic Significance of PDGF, EphA7, CCR5, and CCL5 Levels in Colorectal Cancer. (nih.gov)
- 34. Cytokine CCL5 and receptor CCR5 axis in glioblastoma multiforme. (nih.gov)
- 35. Augmented CCL5/CCR5 signaling in brown adipose tissue inhibits adaptive thermogenesis and worsens insulin resistance in obesity. (nih.gov)
Proteins1
- Chemokines form a superfamily of secreted proteins involved in immunoregulatory and inflammatory processes. (nih.gov)
LYMPHOCYTES1
- In addition, our western blotting study further revealed that the GLE treatment caused an increase in expression of CCL5 chemokine in the cultured B-lymphocytes. (nih.gov)
Inflammation1
- Thus, modulation of EAE with C-C chemokine DNA vaccines is determined by targeting chemokines that are highly transcribed at the site of inflammation at the onset of disease. (medscape.com)
Immune2
- In next part of the review, various chemokines with their specific role in altering immune response to combat various diseases especially cancers will be discussed. (medscape.com)
- Generation of in vivo immune response to CCL5 pDNA had no remarkable effect on EAE. (medscape.com)
Cells1
- 33. Infiltrating CD4+ T cells attenuate chemotherapy sensitivity in prostate cancer via CCL5 signaling. (nih.gov)