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
Expression and cellular localization of the CC chemokines PARC and ELC in human atherosclerotic plaques. (1/347)
Local immune responses are thought to play an important role in the development of atherosclerosis. Histological studies have shown that human atherosclerotic lesions contain T lymphocytes throughout all stages of development, many of which are in an activated state. A number of novel CC chemokines have been described recently, which are potent chemoattractants for lymphocytes: PARC (pulmonary and activation-regulated chemokine), ELC (EBI1-ligand chemokine), LARC (liver and activation-regulated chemokine), and SLC (secondary lymphoid-tissue chemokine). Using reverse transcriptase-polymerase chain reaction and in situ hybridization, we have found gene expression for PARC and ELC but not for LARC or SLC in human atherosclerotic plaques. Immunohistochemical staining of serial plaque sections with specific cell markers revealed highly different expression patterns of PARC and ELC. PARC mRNA was restricted to CD68+ macrophages (n = 14 of 18), whereas ELC mRNA was widely expressed by macrophages and intimal smooth muscle cells (SMC) in nearly all of the lesions examined (n = 12 of 14). ELC mRNA was also found to be expressed in the medial SMC wall of highly calcified plaques (n = 4). Very low levels of ELC mRNA expression could also be detected in normal mammary arteries but no mRNA expression for PARC was detected in these vessels (n = 4). In vitro, ELC mRNA was found to be up-regulated in aortic SMC stimulated with tumor necrosis factor-a and interferon-gamma but not in SMC stimulated with serum. Both PARC and ELC mRNA were expressed by monocyte-derived macrophages but not monocytes. The expression patterns of PARC and ELC mRNA in human atherosclerotic lesions suggest a potential role for these two recently described CC chemokines in attracting T lymphocytes into atherosclerotic lesions. (+info)Cutting edge: secondary lymphoid-tissue chemokine (SLC) and CC chemokine receptor 7 (CCR7) participate in the emigration pathway of mature dendritic cells from the skin to regional lymph nodes. (2/347)
Dendritic cells (DCs) emigrate to regional lymph nodes (LNs) during immune responses via afferent lymphatic channels. Secondary lymphoid-tissue chemokine (SLC), a CC chemokine, is expressed in secondary lymphoid organs and mediates the chemotaxis of lymphocytes and DCs via its receptor, CC chemokine receptor 7 (CCR7). By dual-label fluorescence confocal microscopy, we showed MHC class II-positive cells within SLC-staining lymphatic channels in the mouse dermis. SLC was a potent in vitro chemoattractant for cultured, migratory skin DCs, and it enhanced the emigration of MHC class II-positive DCs from mouse skin explants by an average of 2.5-fold. Mature or cytokine-activated, but not resting, Langerhans cells expressed CCR7 mRNA by RT-PCR. Anti-SLC Abs, but not control or anti-eotaxin Abs, blocked the in vivo migration of 51Cr-labeled, skin-derived DCs from footpads to draining LNs by 50% (n = 9, p < 0. 005). Thus, we provide direct evidence that SLC and CCR7 participate in the emigration of DCs from peripheral tissue to LNs via lymphatics. (+info)Cutting edge: species specificity of the CC chemokine 6Ckine signaling through the CXC chemokine receptor CXCR3: human 6Ckine is not a ligand for the human or mouse CXCR3 receptors. (3/347)
The CC chemokine known as 6Ckine (SLC, Exodus-2, or TCA4) has been identified as a ligand for CCR7. Mouse 6Ckine has also been shown to signal through mouse CXCR3 and share some of the activities of IFN-gamma inducible protein 10 and monokine induced by IFN-gamma. Nonetheless, human 6Ckine has not been shown to bind CXCR3 receptor or have angiostatic activity. In this study, we report that human 6Ckine does not induce a calcium flux in either human CXCR3 or mouse CXCR3 transfected cells, although it is an equally potent agonist as mouse 6Ckine and human macrophage inflammatory protein-3beta in human CCR7 transfected cells. Mouse 6Ckine (but not human 6Ckine) is capable of competing with radiolabeled IFN-gamma inducible protein 10 for human CXCR3. In addition, radiolabeled human 6Ckine does not bind to either human CXCR3 or mouse CXCR3. Together these data suggest that human CC chemokine 6Ckine is not a ligand for the human or mouse CXC chemokine receptor CXCR3. (+info)The CC chemokine receptor-7 ligands 6Ckine and macrophage inflammatory protein-3 beta are potent chemoattractants for in vitro- and in vivo-derived dendritic cells. (4/347)
Dendritic cell migration to secondary lymphoid tissues is critical for Ag presentation to T cells necessary to elicit an immune response. Despite the importance of dendritic cell trafficking in immunity, at present little is understood about the mechanisms that underlie this phenomenon. Using a novel transwell chemotaxis assay system, we demonstrate that the CC chemokine receptor-7 (CCR7) ligands 6Ckine and macrophage inflammatory protein (MIP)-3 beta are selective chemoattractants for MHC class IIhigh B7-2high bone marrow-derived dendritic cells at a potency 1000-fold higher than their known activity on naive T cells. Furthermore, these chemokines stimulate the chemotaxis of freshly isolated lymph node dendritic cells, as well as the egress of skin dendritic cells ex vivo. Because these chemokines are expressed in lymphoid organs and 6Ckine has been localized to high endothelial venules and lymphatic endothelium, we propose that they may play an important role in the homing of dendritic cells to lymphoid tissues. (+info)Secondary lymphoid-tissue chemokine (SLC) is chemotactic for mature dendritic cells. (5/347)
Dendritic cells (DC) take up antigen from the periphery and migrate to the lymphoid organs where they present the processed antigens to T cells. The propensity of DC to migrate changes during DC maturation and is probably dependent on alterations in the expression of chemokine receptors on the surface of DC. Secondary lymphoid tissue chemokine (SLC), a recently discovered chemokine for naive T cells, is primarily expressed in secondary lymphoid organs and may be important for colocalizing T cells with other cell types important for T-cell activation. We show here that SLC is a potent chemokine for mature DC but does not act on immature DC. SLC also induced calcium mobilization specifically in mature DC. SLC and Epstein-Barr virus-induced molecule 1 ligand chemokine completely cross-desensitized the calcium response of each other, indicating that they share similar signaling pathways in DC. The finding that SLC is a potent chemokine for DC as well as naive T cells suggests that it plays a role in colocalizing these two cell types leading to cognate T-cell activation. (+info)Cutting edge: developmental switches in chemokine responses during T cell maturation. (6/347)
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)SLC/exodus2/6Ckine/TCA4 induces chemotaxis of hematopoietic progenitor cells: differential activity of ligands of CCR7, CXCR3, or CXCR4 in chemotaxis vs. suppression of progenitor proliferation. (7/347)
Chemokines induce chemotaxis of hematopoietic progenitor cells (HPC), and suppress their proliferation. In this study we report that SLC/ Exodus2/6Ckine/TCA4 (hereafter termed SLC) is a chemoattractant for human CD34+ HPC. SLC mainly induces preferential chemotaxis of macrophage progenitors. We examined the chemotactic activity of CXCR3 ligands on CD34+ HPC because it has been reported that SLC is a potential ligand of CXC chemokine receptor, CXCR3, in addition to a CC chemokine receptor, CCR7. It was found that the CXCR3 ligands, MIG and interferon-gamma inducible protein-10 (IP-10), unlike SLC, did not induce chemotaxis of CD34+ HPC. In this regard, CCR7 ligands (SLC and CKbeta-11), but not IP-10 and MIG, induce actin polymerization in CD34+ cells. On the other hand, CCR7 ligands and CXCR3 ligands, but not the CXCR4 ligand SDF-1, showed inhibitory activity for proliferation of myeloid progenitor cells. Our results suggest that SLC is a potential trafficking factor for HPC, and that chemokines that bind CCR7, CXCR4, and CXCR3 have differential biological activities on HPC in terms of suppression and chemotaxis. (+info)In vivo-activated CD4 T cells upregulate CXC chemokine receptor 5 and reprogram their response to lymphoid chemokines. (8/347)
Migration of antigen-activated CD4 T cells to B cell areas of lymphoid tissues is important for mounting T cell-dependent antibody responses. Here we show that CXC chemokine receptor (CXCR)5, the receptor for B lymphocyte chemoattractant (BLC), is upregulated on antigen-specific CD4 T cells in vivo when animals are immunized under conditions that promote T cell migration to follicles. In situ hybridization of secondary follicles for BLC showed high expression in mantle zones and low expression in germinal centers. When tested directly ex vivo, CXCR5(hi) T cells exhibited a vigorous chemotactic response to BLC. At the same time, the CXCR5(hi) cells showed reduced responsiveness to the T zone chemokines, Epstein-Barr virus-induced molecule 1 (EBI-1) ligand chemokine (ELC) and secondary lymphoid tissue chemokine (SLC). After adoptive transfer, CXCR5(hi) CD4 T cells did not migrate to follicles, indicating that additional changes may occur after immunization that help direct T cells to follicles. To further explore whether T cells could acquire an intrinsic ability to migrate to follicles, CD4(-)CD8(-) double negative (DN) T cells from MRL-lpr mice were studied. These T cells normally accumulate within follicles of MRL-lpr mice. Upon transfer to wild-type recipients, DN T cells migrated to follicle proximal regions in all secondary lymphoid tissues. Taken together, our findings indicate that reprogramming of responsiveness to constitutively expressed lymphoid tissue chemokines plays an important role in T cell migration to the B cell compartment of lymphoid tissues. (+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.
Vault (organelle)
High endothelial venules
Leonard H. Rome
Chemokine
Lymph node stromal cell
CC chemokine receptors
Allodynia
Haptotaxis
Neuropathic pain
C-C chemokine receptor type 7
CCRL1
Medullary thymic epithelial cells
CCL21
Survivin
Cortical thymic epithelial cells
Chromosome 9
Index of immunology articles
Dock2
Sharon Lewin
CCL19
2014 Ju-Jitsu World Championships
Bolley Johnson
Don't Say No
Dewoitine D.371
Noor-ul-Ain
Benoist Land Tractor Type XII
Santa Cruz Barillas
Maria Margaret Pollen
Ronald Fogleman
Peachtree Street (song)
NOT-CA-10-025: Administrative Supplements to Advance Special Translational Research Acceleration Projects on Immune Response...
Unique Clinical, Immune, and Genetic Signature in Patients with Borrelial Meningoradiculoneuritis - Volume 28, Number 4-April...
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Cross-talk between Colon Cells and Macrophages Increases ST6GALNAC1 and MUC1-sTn Expression in Ulcerative Colitis and Colitis...
CCL21 induces extensive intratumoral immune cell infiltration and specific anti-tumor cellular immunity.
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金子 周一 - 金沢大学研究者情報
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Chemokine CCL5 | Profiles RNS
CRISPR/Cas9-mediated deletion of Interleukin-30 suppresses IGF1 and CXCL5 and boosts SOCS3 reducing prostate cancer growth and...
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Leukemia inhibitory factor - wikidoc
TERM
Receptors2
- A CC-type chemokine with specificity for CCR7 RECEPTORS . (nih.gov)
- CCR receptors with specificity for CHEMOKINE CCL19 and CHEMOKINE CCL21. (bvsalud.org)
CCL19 and CCL212
- CCR7 is a chemokine receptor expressed on the surfaces of T cells, B cells, and mature dendritic cells that controls cell migration in response to the cognate ligands CCL19 and CCL21. (nih.gov)
- Contribution of homeostatic chemokines CCL19 and CCL21 and their receptor CCR7 to coronary artery disease. (cdc.gov)
Receptor5
- 4. Chemotrap-1: an engineered soluble receptor that blocks chemokine-induced migration of metastatic cancer cells in vivo. (nih.gov)
- 5. CCL21 chemokine regulates chemokine receptor CCR7 bearing malignant melanoma cells. (nih.gov)
- Binds to atypical chemokine receptor ACKR4 and mediates the recruitment of beta-arrestin (ARRB1/2) to ACKR4. (nih.gov)
- Polymorphism in the chemokine receptor 7 gene (CCR7) is associated with previous myocardial infarction in patients undergoing elective coronary angiography. (cdc.gov)
- The TSLP receptor (TSLPR) complex consists of a heterodimer of the IL-7 receptor chain (IL-7R) and TSLPR.4-7 In humans, TSLPR is highly expressed by myeloid DCs (mDCs), and TSLP produced by epitherial cells strongly activates mDCs to upregulate MHC class II and co-stimulatory molecules, improve survival, and produce a variety of chemokines, such as CCL-17 (TARC) and CCL-21 (MDC). (insulin-receptor.info)
Motif chemokine ligand2
- When stratified by specific clinical manifestation, patients with meningoradiculoneuritis had higher levels of B-cell chemoattractants CXC motif chemokine ligand (CXCL) 12 and CXCL13 and T-cell-associated mediators CXCL9, CXCL10, and interleukin 17, compared with those without radicular pain. (cdc.gov)
- C-C motif chemokine ligand 21 [So. (gsea-msigdb.org)
Ligand2
- Purpose of review We review P-selectin glycoprotein ligand-1 (PSGL-1) as a selectin and chemokine-binding adhesion molecule. (elsevierpure.com)
- Recent findings PSGL-1 was originally described as a leukocyte ligand for P-selectin, but it is actually a ligand for all selectins (P-, L-and E-selectin), binds chemokines, activates integrins and profoundly affects T-cell biology. (elsevierpure.com)
Cytokines1
- Macrophage Inflammatory Protein MIP-1 alpha is part of the CC subfamily of the chemokine superfamily of chemoattractant cytokines. (creativebiomart.net)
Lymphoid4
- 8. Tobacco exposure primes the secretion of CCL21 positively associated with tertiary lymphoid structure and response to immunotherapy. (nih.gov)
- The chemokine CCL21 is normally expressed in secondary lymphoid organs and acts as a chemoattractant for several populations of immune cells. (nih.gov)
- Detailed flow cytometric and confocal analysis of CCL21-treated tumor cell isolates revealed increased lymphoid-related dendritic cells (lDC) and myeloid DC (mDC), naïve and mature T cells, natural killer (NK) cells, and NKT cells infiltrating the tumor mass. (nih.gov)
- PSGL-1 also plays a crucial role in T-cell homeostasis by binding to lymphoid chemokines, and can induce tolerance by enhancing the functions of regulatory T cells. (elsevierpure.com)
6Ckine1
- CCL21/6Ckine " has 16 results in Products. (rndsystems.com)
Coronary artery1
- The soluble chemokine is elevated in rheumatoid arthritis synovial fluid and in the serum of coronary artery disease patients. (rndsystems.com)
Murine2
- 10. Low-dose paclitaxel improves the therapeutic efficacy of recombinant adenovirus encoding CCL21 chemokine against murine cancer. (nih.gov)
- Herein, we report that intratumoral CCL21 administration recruited significant numbers of immune cells into murine pancreatic tumors and inhibited tumor growth. (nih.gov)
Ligands1
- Sequence variation in promoter regions of genes for CC chemokine ligands (CCL)19 and 21 in Czech patients with myocardial infarction. (cdc.gov)
Tumor growth2
- 6. Salmonella typhimurium engineered to produce CCL21 inhibit tumor growth. (nih.gov)
- Furthermore, CCL21 intratumoral treatments resulted in significant tumor growth inhibition in wild-type (WT) C57BL/6 mice, but no therapeutic benefit was observed in C57BL/6 RAG2-/-Pfp-/- mice, suggesting that the growth inhibition observed was immunologically mediated. (nih.gov)
CCL53
- Chemokine CCL5" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (wakehealth.edu)
- This graph shows the total number of publications written about "Chemokine CCL5" by people in this website by year, and whether "Chemokine CCL5" was a major or minor topic of these publications. (wakehealth.edu)
- Below are the most recent publications written about "Chemokine CCL5" by people in Profiles. (wakehealth.edu)
Signaling1
- 1. Chemokine Analysis in Patients with Metastatic Uveal Melanoma Suggests a Role for CCL21 Signaling in Combined Epigenetic Therapy and Checkpoint Immunotherapy. (nih.gov)
DENDRITIC CELLS2
- In response to infection, expression of CCL19 and expression of CCL21 were oppositely regulated, and myeloid dendritic cells upregulated CCR7 expression. (nih.gov)
- CCL21 is constitutively presented on initial lymphatic vessels, high endothelial venules (HEV), and lymph node dendritic cells (DC) where it promotes the docking of DC to lymphatic vessels and the retention of T cells by lymph node DC, resulting in T cell priming for activation. (rndsystems.com)
Protein1
- Similar to other chemokines the protein encoded by this gene inhibits hemopoiesis and stimulates chemotaxis. (nih.gov)
Gene1
- 12. A 12-chemokine gene signature is associated with the enhanced immunogram scores and is relevant for precision immunotherapy. (nih.gov)
Especificidad1
- Receptores CCR con especificidad para la QUIMIOQUINA CCL19 y la QUIMIOQUINA CCL21. (bvsalud.org)
Immune4
- CCL21 induces extensive intratumoral immune cell infiltration and specific anti-tumor cellular immunity. (nih.gov)
- Chemokines are vital messengers that regulate immune cell activity. (nih.gov)
- CCL21 intratumoral injections generated immune responses that were tumor-specific and that could be transferred to naïve animals via splenocytes. (nih.gov)
- Thus, these data demonstrate in a pancreatic tumor model that intratumoral administration of CCL21 can cause significant immune cell infiltration of the tumor mass, delay growth of treated tumors, and generate a tumor-specific cellular immune response. (nih.gov)
Function1
- Shape and Function of Interstitial Chemokine CCL21 Gradients Are Independent of Heparan Sulfates Produced by Lymphatic Endothelium. (ista.ac.at)
Patients1
- 13. A phase I/randomized phase II study of GM.CD40L vaccine in combination with CCL21 in patients with advanced lung adenocarcinoma. (nih.gov)