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
Selective recruitment of CCR4-bearing Th2 cells toward antigen-presenting cells by the CC chemokines thymus and activation-regulated chemokine and macrophage-derived chemokine. (1/183)
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)Chemokine Up-regulation and activated T cell attraction by maturing dendritic cells. (2/183)
Langerhans' cells migrating from contact-sensitized skin were found to up-regulate expression of macrophage-derived chemokine (MDC) during maturation into lymph node dendritic cells (DCs). Naive T cells did not migrate toward MDC, but antigen-specific T cells rapidly acquired MDC responsiveness in vivo after a subcutaneous injection of antigen. In chemotaxis assays, maturing DCs attracted activated T cells more strongly than naive T cells. These studies identified chemokine up-regulation as part of the Langerhans' cell maturation program to immunogenic T cell-zone DC. Preferential recruitment of activated T cells may be a mechanism used by maturing DCs to promote encounters with antigen-specific T cells. (+info)Mouse monocyte-derived chemokine is involved in airway hyperreactivity and lung inflammation. (3/183)
The cloning, expression, and function of the murine (m) homologue of human (h) monocyte-derived chemokine (MDC) is reported here. Like hMDC, mMDC is able to elicit the chemotactic migration in vitro of activated lymphocytes and monocytes. Among activated lymphocytes, Th2 cells were induced to migrate most efficiently. mMDC mRNA and protein expression is modulated during the course of an allergic reaction in the lung. Neutralization of mMDC with specific Abs in a model of lung inflammation resulted in prevention of airway hyperreactivity and significant reduction of eosinophils in the lung interstitium but not in the airway lumen. These data suggest that mMDC is essential in the transit/retention of leukocytes in the lung tissue rather than in their extravasation from the blood vessel or during their transepithelial migration into the airways. These results also highlight the relevance of factors, such as mMDC, that regulate the migration and accumulation of leukocytes within the tissue during the development of the key physiological endpoint of asthma, airway hyperreactivity. (+info)Cutting edge: developmental switches in chemokine responses during T cell maturation. (4/183)
We show that developmental transitions during thymocyte maturation are associated with dramatic changes in chemotactic responses to chemokines. Macrophage-derived chemokine, a chemokine expressed in the thymic medulla, attracts thymocytes only during a brief window of development, between the late cortical and early medullary stages. All medullary phenotypes (CD4 or CD8 single positive) but not immature thymocytes respond to the medullary stroma-expressed (and secondary lymphoid tissue-associated) chemokines secondary lymphoid-tissue chemokine and macrophage inflammatory protein-3beta. The appearance of these responses is associated with the phenotypic stage of cortex to medulla migration and with up-regulation of mRNA for the receptors CCR4 (for macrophage-derived chemokine and thymus and activation-regulated chemokine) and CCR7 (for secondary lymphoid-tissue chemokine and macrophage inflammatory protein-3beta). In contrast, most immature and medullary thymocytes migrate to thymus-expressed chemokine, an ability that is lost only with up-regulation of the peripheral homing receptor L-selectin during the latest stages of thymocyte maturation associated with export to the periphery. Developmental switches in chemokine responses may help regulate critical migratory events during T cell development. (+info)Macrophage-derived chemokine is localized to thymic medullary epithelial cells and is a chemoattractant for CD3(+), CD4(+), CD8(low) thymocytes. (5/183)
Macrophage-derived chemokine (MDC) is a recently identified CC chemokine that is a potent chemoattractant for dendritic cells, natural killer (NK) cells, and the Th2 subset of peripheral blood T cells. In normal tissues, MDC mRNA is expressed principally in the thymus. Immunohistochemical analysis performed on 5 human postnatal thymuses showed high MDC immunoreactivity, which was selectively localized to epithelial cells within the medulla. To examine the effects of MDC on immature T cells, we have identified cDNA clones for mouse and rat MDC. Expression of MDC in murine tissues is also highly restricted, with significant levels of mRNA found only in the thymus. Thymocytes express high-affinity binding sites for MDC (kd = 0.7 nmol/L), and, in vitro, MDC is a chemoattractant for these cells. MDC-responsive murine thymocytes express mRNA for CCR4, a recently identified receptor for MDC. Phenotypic analysis of MDC-responsive cells shows that they are enriched for a subset of double-positive cells that express high levels of CD3 and CD4 and that have reduced levels of CD8. This subset of MDC-responsive cells is consistent with the observed expression of MDC within the medulla, because more mature cells are found there. MDC may therefore play a role in the migration of T-cell subsets during development within the thymus. (+info)Differential responsiveness to constitutive vs. inducible chemokines of immature and mature mouse dendritic cells. (6/183)
Upon exposure to immune or inflammatory stimuli, dendritic cells (DC) migrate from peripheral tissues to lymphoid organs, where they present antigen. The molecular basis for the peculiar trafficking properties of DC is largely unknown. In this study, mouse DC were generated from CD34+ bone marrow precursors and cultured with granulocyte-macrophage-CSF and Flt3 ligand for 9 days. Chemokines active on immature DC include MIP1alpha, RANTES, MIP1beta, MCP-1, MCP-3, and the constitutively expressed SDF1, MDC, and ELC. TNF-alpha-induced DC maturation caused reduction of migration to inducible chemokines (MIP1alpha, RANTES, MIP1beta, MCP-1, and MCP-3) and increased migration to SDF1, MDC, and ELC. Similar results were obtained by CD40 ligation or culture in the presence of bacterial lipopolysaccharide. TNF-alpha down-regulated CC chemokine receptor (CCR)1, CCR2, and CCR5 and up-regulated CCR7 mRNA levels, in agreement with functional data. This study shows that selective responsiveness of mature and immature DC to inducible vs. constitutively produced chemokines can contribute to the regulated trafficking of DC. (+info)Overproduction of Th2-specific chemokines in NC/Nga mice exhibiting atopic dermatitis-like lesions. (7/183)
We have examined the expression of chemokines and their receptors in the atopic dermatitis-like (AD-like) lesions of NC/Nga mice. Such lesions develop when the mice are kept in conventional conditions, but not when they are kept isolated from specific pathogens. The thymus- and activation-regulated chemokine TARC is unexpectedly highly expressed in the basal epidermis of 14-week-old mice with lesions, whereas it is not expressed in the skin without lesions. Production of TARC by keratinocytes was confirmed by culturing murine keratinocytic cell line cells (PAM212) with TNF-alpha, IFN-gamma, or IL-1beta. Expression of another Th2 chemokine, macrophage-derived chemokine (MDC), was observed in the skin from mice kept in both conventional and pathogen-free conditions, but expression of MDC was increased severalfold in the skin with lesions. The cellular origin of MDC was identified to be dermal dendritic cells. Infiltration of the skin by IL-4-producing T cells and mast cells, and the increase of CCR4 mRNA in the skin, coincided with the development of AD lesions. These observations indicate that TARC and MDC actively participate in the pathogenesis of AD-like lesions in NC/Nga mice and that these Th2 chemokines could be novel targets for intervention therapy of AD in humans. (+info)Mouse langerhans cells differentially express an activated T cell-attracting CC chemokine. (8/183)
Epidermal Langerhans cells represent an immature population of dendritic cells, not yet able to prime naive T cells. Following in vitro culture Langerhans cells mature into potent immunostimulatory cells. We constructed a representative cDNA library of in vitro matured murine Langerhans cells. Applying a differential screening procedure 112 differentially expressed cDNA clones were isolated. Thirty-six clones represented cDNA fragments of the same gene, identifying it to be the most actively expressed gene induced in maturing Langerhans cells. A full-length cDNA was sequenced completely. The open reading frame codes for a protein of 92 amino acids containing a leader peptide of 24 amino acids, yielding a mature protein of 7.8 kDa molecular weight. Database searches revealed 99.4% sequence identity on the nucleotide level to the recently described mouse CC chemokine ABCD-1, as well as 74% sequence identity to the human CC chemokine, the macrophage-derived chemokine/stimulated T cell chemotactic protein. Expression was analyzed by reverse transcriptase-polymerase chain reaction on a large panel of cell types. Unlike the macrophage-derived chemokine, expression was not detected in macrophages stimulated by various cytokines. Expression is restricted to cultured Langerhans cells, in vitro cultured dendritic cells, and lipopolysaccharide-activated B cells. Recombinant protein was expressed in the yeast Pichia pastoris and purified to homogeneity. Whereas no chemotactic activity was observed in chemotaxis assays for naive T cells, B cells, cultured dendritic cells, and Langerhans cells, a strong chemoattractant activity was exerted on activated T cells. Thus, production of this chemokine by dendritic cells may be essential for the establishment and amplification of T cell responses. (+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.
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Macrophage-derived chemokine2
- 8. Macrophage-derived chemokine CCL22 and regulatory T cells in ovarian cancer patients. (nih.gov)
- To achieve this goal this study designed a prototype chemokine-based DNA epitope vaccine expressing a fusion protein that consists of 3 copies of the self-B cell epitope of Aβ42 (Aβ1-11) , a non-self T helper cell epitope (PADRE), and macrophage-derived chemokine (MDC/CCL22) as a molecular adjuvant to promote a strong antiinflammatory Th2 phenotype. (nih.gov)
CCL17 and CCL228
- CCL17 and CCL22 chemokines are upregulated in human obesity and play a role in vascular dysfunction. (bvsalud.org)
- The aim of this study was to investigate the role of chemokine receptor CCR4 and its ligands CCL17 and CCL22 in human morbid obesity . (bvsalud.org)
- therefore, using this ex vivo transmigration method we examined CCL17- and CCL22-induced movement of CCR4+ lymphocytes. (cdc.gov)
- To establish chemokine gradients, CCL17 and CCL22 were placed in the bottom chamber of the transmigration system. (cdc.gov)
- CCR4 ligands, CCL17 and CCL22, were produced in lymph nodes and skin from dendritic cells, macrophages and Langerhans cells. (nih.gov)
- Functionally, the CCR4-Q330 nonsense isoform was gain-of-function since it increased cell migration towards the CCR4 ligands CCL17 and CCL22, in part by impairing receptor internalization. (nih.gov)
- Quantification of the chemokines CCL17 and CCL22 in human colorectal adenocarcinomas. (cdc.gov)
- This review presents key clinical studies of Multiple sclerosis together with experimental studies in animals that have demonstrated functional roles of CCR4, CCL17, and CCL22 in experimental autoimmune encephalomyelitis pathogenesis. (cusabio.com)
CCR45
- The product of this gene binds to chemokine receptor CCR4. (nih.gov)
- A CC-type chemokine with specificity for CCR4 RECEPTORS . (nih.gov)
- High expression of CC chemokine receptor 4 (CCR4) has been identified as a hallmark gene in ATLL. (nih.gov)
- CCR4 is a chemokine receptor, which has a critical role in immune cell trafficking. (nih.gov)
- We report an adult T-cell leukemia-lymphoma (ATL) patient suffering from fatal reactivation of hepatitis B virus (HBV) infection after treatment with the anti-CC chemokine receptor 4 (CCR4) monoclonal antibody, mogamulizumab. (nih.gov)
Cytokines1
- Macrophage Inflammatory Protein MIP-1 alpha is part of the CC subfamily of the chemokine superfamily of chemoattractant cytokines. (creativebiomart.net)
Motif1
- C-C motif chemokine ligand 21 [So. (gsea-msigdb.org)
Receptor3
- This mutant enhanced PI(3) kinase/AKT activation following receptor engagement by CCL22 in ATLL cells, and conferred a growth advantage in long term in vitro cultures. (nih.gov)
- High affinity receptor for the C-C type chemokines CCL17/TARC, CCL22/MDC and CKLF isoform 1/CKLF1. (cusabio.com)
- Chemokine CXC receptor 3 (CXCR3) is the only receptor of CXCL10. (biomedcentral.com)
RECEPTORS1
- the expression of chemokine receptors in different peripheral blood T-cell subsets in patients with polymyositis (PM) and dermatomyositis, was examined. (cusabio.com)
Ligand1
- CXC chemokine ligand 10 (CXCL10) is a kind of lymphocyte chemotactic protein produced by interferon-γ (IFN-γ) or lipopolysaccharide (LPS), also known as interferon-induced protein 10 (IP-10). (biomedcentral.com)
CXCL101
- CSF-NFL was associated with both new T2 lesions and brain volume loss during follow-up, whereas CSF-CHI3L1 was associated mainly with brain volume loss and CXCL1, CXCL10, CXCL13, CCL22, and MMP-9 were associated mainly with new T2 lesions. (biomedcentral.com)
TARC1
- In advanced human plaques increased numbers of DCs are found in clusters with T cells, and DC-derived chemokines, such as CCL17 (also known as TARC/ thymus- and activation-regulated chemokine ), can be detected in atherosclerotic lesions. (hindawi.com)
Cytokine1
- The study findings also lead to the possibility of using TLR4 antagonists such as Eritoran to reduce cytokine/chemokine production and alleviate disease symptoms. (thailandmedical.news)
Dendritic cells2
- Human CCL22 is expressed in dendritic cells, macrophages and activated monocytes. (rndsystems.com)
- Recombinant or chemically synthesized mature CCL22 has been shown to induce chemotaxis or Ca 2+ mobilization in dendritic cells, IL-2 activated NK cells, and activated T lymphocytes. (rndsystems.com)
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)
Thymus1
- In addition, CCL22 expression is also detected in the tissues of thymus, lymph node and appendix. (rndsystems.com)
Protein5
- CCL22, also named stimulated T cell chemotactic protein (STCP-1), is a CC chemokine initially isolated from clones of monocyte-derived macrophages. (rndsystems.com)
- Human CCL22 cDNA encodes a precursor protein of 93 amino acid residues with a 24 amino acid residue predicted signal peptide that is cleaved to yield a 69 amino acid residue mature 8 kDa protein. (rndsystems.com)
- Based on amino-terminal sequence analysis, the major CD8 + T lymphocyte-derived CCL22 protein yielded an amino-terminal sequence of YGANM, which is two amino acid residues shorter than the predicted mature CCL22. (rndsystems.com)
- French Study Shows That SARS-CoV-2 Envelope Protein (E) Binds And Activates TLR2 And Causes Production Of CXCL8 Inflammatory Chemokine! (thailandmedical.news)
- A new study by French researchers from INSERM, CNRS and Université Paul Sabatier along with scientific support from the University of California Irvine-USA have discovered that the SARS-CoV-2 Envelope Protein (E) binds and activates TLR2 and causes production of CXCL8 inflammatory chemokine. (thailandmedical.news)
Lymphocytes2
- This chemokine may play a role in the trafficking of activated T lymphocytes to inflammatory sites and other aspects of activated T lymphocyte physiology. (nih.gov)
- Isolated lymphocytes were then added to top chambers and over a 48 h period the lymphocytes actively migrated through 3 µm pores towards the chemokine in the bottom chamber. (cdc.gov)
Regulatory2
- Poly(lactic-co-glycolic) acid (PLGA) controlled release microparticles were fabricated using a double emulsion procedure to encapsulate and sustain a biological gradient of the regulatory lymphocyte recruiting chemokine, CCL-22. (umich.edu)
- We observed the recruitment of regulatory T cells to CCL22 microparticles (injected into the periodontium) in mice and the subsequent amelioration of disease symptoms. (umich.edu)
Proteins1
- Besides the well-known chemokine CCL17 other proteins i.e. (21docs.com)
Significantly1
- CCL13, CCL22, E-selectin and BDNF were differently regulated and significantly associated with treatment response. (21docs.com)
Human2
- Detects human CCL22/MDC in ELISAs and Western blots. (rndsystems.com)
- The gene for human CCL22 has been mapped to chromosome 16 rather than chromosome 17 where the genes for many human CC chemokines are clustered. (rndsystems.com)
Expression1
- CCL22 treated animals had less alveolar bone resorption and lower expression of inflammatory mediators than controls. (umich.edu)
Roles1
- Chemokines are known to play critical roles mediating inflammation in many pathophysiological processes. (bvsalud.org)
Cell1
- A CD8 + T lymphocyte-derived secreted soluble activity that suppresses infection by primary non-syncytium-inducing and syncytium-inducing HIV-1 isolates and the T-cell line-adapted isolate HIV-1 IIIB , has been identified as CCL22. (rndsystems.com)
Family1
- At the amino acid sequence level, CCL22 shows less than 35% identity to other CC chemokine family members. (rndsystems.com)
General1
- In general, the method is effective if the chemokine of interest is consistently generating chemokinetics at a statistically higher level than the media control. (cdc.gov)
Study2
- cutánea maligna de células T. Luego se realizó el frotis de médula ósea, en el que se identificaron células «cerebriformes» study conception, manuscript que confirmaron el diagnóstico de síndrome de Sézary. (bvsalud.org)
- Furthermore, the study findings showed that this interaction is able to engage TLR2 pathway as demonstrated by its capacity to activate NF-κB transcription factor and to stimulate the production of CXCL8 inflammatory chemokine in a TLR2-dependent manner. (thailandmedical.news)