Macrophage Inflammatory Proteins
Gene Expression Regulation
Reverse Transcriptase Polymerase Chain Reaction
Enzyme-Linked Immunosorbent Assay
Monocyte Chemoattractant Proteins
Disease Models, Animal
Tumor Necrosis Factor-alpha
Duffy Blood-Group System
Chemotactic Factors, Eosinophil
Cell Migration Inhibition
Molecular Sequence Data
Intercellular Signaling Peptides and Proteins
Amino Acid Sequence
Gene Expression Profiling
Platelet Factor 4
Bronchoalveolar Lavage Fluid
Drug-Induced Liver Injury
Molecular cloning of a novel CC chemokine, interleukin-11 receptor alpha-locus chemokine (ILC), which is located on chromosome 9p13 and a potential homologue of a CC chemokine encoded by molluscum contagiosum virus. (1/35)Molluscum contagiosum virus (MCV) encodes a CC chemokine MC148R which is likely to have been acquired from the host. By a homology search employing MC148R as a probe, we have identified a novel CC chemokine whose gene exists next to the IL-11 receptor alpha (IL-11Ralpha) gene in both humans and mice. Thus, this chemokine maps to chromosome 9p13 in humans where IL-11Ralpha has been assigned. We term this novel chemokine IL-11Ralpha-locus chemokine (ILC). ILC has the highest homology to MC148R among the known human CC chemokines. Furthermore, ILC is strongly and selectively expressed in the skin where infection of MCV also takes place. Thus, ILC is likely to be the original chemokine of MC148R. (+info)
ESkine, a novel beta-chemokine, is differentially spliced to produce secretable and nuclear targeted isoforms. (2/35)Using the murine embryonal stem cell system, we have identified a novel gene encoding a highly divergent member of the beta-chemokine family of proinflammatory mediators and have called this protein ESkine. Much of the coding sequence for ESkine overlaps with the 3'-end of a novel interleukin 11 receptor alpha-like sequence on murine chromosome 4. ESkine is produced as two splice variants. One of these variants encodes a classical chemokine with an associated signal peptide, while the other variant (PESKY) possesses the main body of the chemokine but has replaced the signal peptide with an alternative stretch of amino acids that allows for nuclear targeting of this isoform. This differential splicing arises as a result of alternative 5' exon usage. These differentially spliced forms are expressed at discrete tissue loci. Thus, while ESkine is highly expressed in the placenta, PESKY is mainly expressed in the Testes and brain and weakly in the developing embryo. Studies on the proinflammatory properties of ESkine reveal it to be active in inducing polarization of CD4(+) T cells but to be inactive on other hemopoietic cellular populations. (+info)
Cutting edge: identification of the orphan receptor G-protein-coupled receptor 2 as CCR10, a specific receptor for the chemokine ESkine. (3/35)A number of orphan G-protein coupled receptors (GPR) have been reported as putative chemokine receptors. One previously reported orphan receptor is an incomplete PCR clone, called GPR2. Here we report the cloning of full-length human (h)GPR2 and mouse (m)GPR2 cDNAs, and the identification of GPR2 as a receptor for a novel CC chemokine called ESkine. hGPR2 is expressed at high levels in testis and small intestine, and at lower levels in other tissues. mGPR2 was expressed at high levels in small intestine, colon, lymph nodes, and Peyer's patches and at lower levels in thymus and spleen. Stimulation of L1.2/hGPR2 transfectants with hESkine induced their migration and resulted in intracellular calcium mobilization. These results provide evidence that GPR2 is a specific receptor for ESkine. We propose that GPR2 be renamed as CCR10. The expression pattern of mGPR2/CCR10 suggests that it may play a role in the homing/trafficking of leukocytes within intestinal and lymphoid environments. (+info)
Cutting edge: the orphan chemokine receptor G protein-coupled receptor-2 (GPR-2, CCR10) binds the skin-associated chemokine CCL27 (CTACK/ALP/ILC). (4/35)We recently reported the identification of a chemokine (CTACK), which has been renamed CCL27 according to a new systematic chemokine nomenclature. We report that CCL27 binds the previously orphan chemokine receptor GPR-2, as detected by calcium flux and chemotactic responses of GPR-2 transfectants. We renamed this receptor CCR10. Because of the skin-associated expression pattern of CCL27, we focused on the expression of CCL27 and CCR10 in normal skin compared with inflammatory and autoimmune skin diseases. CCL27 is constitutively produced by keratinocytes but can also be induced upon stimulation with TNF-alpha and IL-1beta. CCR10 is not expressed by keratinocytes and is instead expressed by melanocytes, dermal fibroblasts, and dermal microvascular endothelial cells. CCR10 was also detected in T cells as well as in skin-derived Langerhans cells. Taken together, these observations suggest a role for this novel ligand/receptor pair in both skin homeostasis as well as a potential role in inflammatory responses. (+info)
DNAWorks: an automated method for designing oligonucleotides for PCR-based gene synthesis. (5/35)The availability of sequences of entire genomes has dramatically increased the number of protein targets, many of which will need to be overexpressed in cells other than the original source of DNA. Gene synthesis often provides a fast and economically efficient approach. The synthetic gene can be optimized for expression and constructed for easy mutational manipulation without regard to the parent genome. Yet design and construction of synthetic genes, especially those coding for large proteins, can be a slow, difficult and confusing process. We have written a computer program that automates the design of oligonucleotides for gene synthesis. Our program requires simple input information, i.e. amino acid sequence of the target protein and melting temperature (needed for the gene assembly) of synthetic oligonucleotides. The program outputs a series of oligonucleotide sequences with codons optimized for expression in an organism of choice. Those oligonucleotides are characterized by highly homogeneous melting temperatures and a minimized tendency for hairpin formation. With the help of this program and a two-step PCR method, we have successfully constructed numerous synthetic genes, ranging from 139 to 1042 bp. The approach presented here simplifies the production of proteins from a wide variety of organisms for genomics-based studies. (+info)
The chemokine ESkine/CCL27 displays novel modes of intracrine and paracrine function. (6/35)We have previously shown that the beta-chemokine ESkine/CCL27 is differentially spliced to produce two alternative forms. One is a secreted chemokine (ESkine), whereas the other (PESKY) lacks a signal peptide and is translocated to the nucleus. The role of this nuclear-targeted chemokine has not so far been defined, and it was the purpose of this study to examine this chemokine variant in more depth. To identify the region of PESKY involved in the nuclear translocation we tagged fragments with enhanced green fluorescent protein and expressed them in Chinese hamster ovary cells. We show PESKY nuclear translocation to be dependent on C-terminal residues that are shared with the signal peptide-bearing variant ESkine. Indeed we further demonstrate that ESkine can also use these C-terminal residues to enter the nucleus of cells following receptor (CCR10)-mediated internalization. To examine biological roles for PESKY we have overexpressed it in 3T3 cells. Such overexpression results in marked cytoskeletal rearrangements that are coincident with a radical reorganization of the cellular actin cytoskeleton. Microarray analyses and Ab neutralization studies indicate that these changes are mediated in part by insulin-like growth factor-1. Furthermore, monolayer wounding assays indicate that PESKY expression correlates with markedly increased migratory capacity. Thus, it is our contention that nuclear PESKY and ESkine both enter the nucleus by either intracrine or paracrine mechanisms and may facilitate cellular migration by inducing actin cytoskeletal relaxation. Therefore, nuclear ESkine/PESKY represents a novel paradigm for chemokine function. (+info)
CCR4 versus CCR10 in human cutaneous TH lymphocyte trafficking. (7/35)The chemokine receptors (CCRs) CCR4 and CCR10, and the cutaneous lymphocyte antigen (CLA), have each been proposed as critical mediators of skin-specific TH lymphocyte homing in mice and humans. CLA initiates skin homing by mediating E-selectin-dependent tethering and rolling within cutaneous venules, but the specific roles of CCR4 and CCR10 are unclear. We have generated an antihuman CCR10 monoclonal antibody (mAb; 1B5) to illuminate the individual contributions of these molecules. This mAb allows us to compare CCR10, CCR4, and CLA expression within human TH populations. The mAb 1B5 recognizes functional CCR10 expression, as chemotactic responsiveness to cutaneous T-cell-attracting chemokine (CTACK)/CCL27 (a CCR10 ligand) parallels the staining of TH subsets. We find CCR10 expressed by only a minority (approximately 30%) of blood-borne, skin-homing (CLA+/CCR4+) TH cells. However, essentially all members of the relatively small "effector" (CLA+/CCR4+/CD27-/CCR7-) skin-homing TH population express CCR10. Most skin-infiltrating lymphocytes in allergic delayed-type hypersensitivity (DTH) and bacterial chancroid skin lesions express both CCR4 and CLA, but only about 10% express CCR10. This suggests for the 2 models of TH skin homing studied here that CCR10+ TH cells have no advantage over other CLA+/CCR4+ TH cells in homing to cutaneous sites. We conclude that the skin-homing TH compartment is itself divided into distinct subpopulations, the smaller of which expresses both CCR4 and CCR10, and the larger of which expresses only CCR4. Thus, CCR10 is unlikely to be necessary for cutaneous homing of TH cells in the models studied here. CCR10 may instead play a role in the movement of specialized "effector" cutaneous TH cells to and/or within epidermal microenvironments. (+info)
Antitumor effect by interleukin-11 receptor alpha-locus chemokine/CCL27, introduced into tumor cells through a recombinant adenovirus vector. (8/35)In this study, we examined antitumor activity of a mouse CC chemokine ILC/CCL27 and a mouse CX(3)C chemokine fractalkine/CX(3)CL1 in vivo. We generated recombinant adenovirus vectors with a fiber mutation, encoding mILC (Ad-RGD-mILC) and mFKN (Ad-RGD-mFKN). We confirmed tumor cells infected with Ad-RGD-mILC and Ad-RGD-mFKN to express and release these chemokines. Tumor rejection experiments in vivo were carried out by inoculating OV-HM cells infected with Ad-RGD-mILC or Ad-RGD-mFKN into immunocompetent mice. mILC significantly suppressed the tumor growth, whereas no such significant effect was observed by mFKN. The antitumor activity induced by mILC was T cell dependent, involving both CD4(+) and CD8(+) T cells. Immunohistochemical analysis revealed accumulation of both CD3(+) lymphocytes and NK cells in the tumor tissue transduced with mILC and mFKN. However, there was a significant difference in the distribution of infiltrating cells. Furthermore, mFKN appeared to have an angiogenic activity, which might have masked its tumor suppressive activity. Collectively, ILC/CCL27 may be a good candidate molecule for cancer gene therapy. (+info)
There are several key features of inflammation:
1. Increased blood flow: Blood vessels in the affected area dilate, allowing more blood to flow into the tissue and bringing with it immune cells, nutrients, and other signaling molecules.
2. Leukocyte migration: White blood cells, such as neutrophils and monocytes, migrate towards the site of inflammation in response to chemical signals.
3. Release of mediators: Inflammatory mediators, such as cytokines and chemokines, are released by immune cells and other cells in the affected tissue. These molecules help to coordinate the immune response and attract more immune cells to the site of inflammation.
4. Activation of immune cells: Immune cells, such as macrophages and T cells, become activated and start to phagocytose (engulf) pathogens or damaged tissue.
5. Increased heat production: Inflammation can cause an increase in metabolic activity in the affected tissue, leading to increased heat production.
6. Redness and swelling: Increased blood flow and leakiness of blood vessels can cause redness and swelling in the affected area.
7. Pain: Inflammation can cause pain through the activation of nociceptors (pain-sensing neurons) and the release of pro-inflammatory mediators.
Inflammation can be acute or chronic. Acute inflammation is a short-term response to injury or infection, which helps to resolve the issue quickly. Chronic inflammation is a long-term response that can cause ongoing damage and diseases such as arthritis, asthma, and cancer.
There are several types of inflammation, including:
1. Acute inflammation: A short-term response to injury or infection.
2. Chronic inflammation: A long-term response that can cause ongoing damage and diseases.
3. Autoimmune inflammation: An inappropriate immune response against the body's own tissues.
4. Allergic inflammation: An immune response to a harmless substance, such as pollen or dust mites.
5. Parasitic inflammation: An immune response to parasites, such as worms or fungi.
6. Bacterial inflammation: An immune response to bacteria.
7. Viral inflammation: An immune response to viruses.
8. Fungal inflammation: An immune response to fungi.
There are several ways to reduce inflammation, including:
1. Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, and disease-modifying anti-rheumatic drugs (DMARDs).
2. Lifestyle changes, such as a healthy diet, regular exercise, stress management, and getting enough sleep.
3. Alternative therapies, such as acupuncture, herbal supplements, and mind-body practices.
4. Addressing underlying conditions, such as hormonal imbalances, gut health issues, and chronic infections.
5. Using anti-inflammatory compounds found in certain foods, such as omega-3 fatty acids, turmeric, and ginger.
It's important to note that chronic inflammation can lead to a range of health problems, including:
3. Heart disease
5. Alzheimer's disease
6. Parkinson's disease
7. Autoimmune disorders, such as lupus and rheumatoid arthritis.
Therefore, it's important to manage inflammation effectively to prevent these complications and improve overall health and well-being.
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.
C-c motif chemokine ligand 27
CC chemokine receptors
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NDF-RT Code NDF-RT Name
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- Tumor cell invasion share many similarities with leukocyte trafficking, which is critically regulated by chemokines and their receptors. (oncotarget.com)
- Chemokine receptors are cytokine receptors found on the surface of certain cells that interact with a type of cytokine called a chemokine. (oncotarget.com)
- There have been 19 distinct chemokine receptors in mammals. (oncotarget.com)
- Following interaction with their specific chemokine ligands, chemokine receptors trigger a flux in intracellular calcium (Ca2+) ions (calcium signaling). (oncotarget.com)
- A CC-type chemokine with specificity for CCR10 RECEPTORS . (nih.gov)
- Chemokine receptors comprise a large subfamily of 7TM proteins that bind one or more chemokines, a large family of small cytokines typically possessing chemotactic activity for leukocytes. (tansobio.com)
- Chemokine receptors can be divided by function into two main groups: G protein-coupled chemokine receptors, which mediate leukocyte trafficking, and "Atypical chemokine receptors", which may signal through non-G protein-coupled mechanisms and act as chemokine scavengers to downregulate inflammation or shape chemokine gradients . (tansobio.com)
- Most chemokine receptors are able to bind multiple high-affinity chemokine ligands, but the ligands for a given receptor are almost always restricted to the same structural subclass. (tansobio.com)
- Receptors for inflammatory chemokines are typically highly promiscuous with regard to ligand specificity, and may lack a selective endogenous ligand. (tansobio.com)
- G protein-coupled chemokine receptors are named acccording to the class of chemokines bound, whereas ACKR is the root acronym for atypical chemokine receptors . (tansobio.com)
- There can be substantial cross-species differences in the sequences of both chemokines and chemokine receptors, and in the pharmacology and biology of chemokine receptors. (tansobio.com)
- Endogenous and microbial non-chemokine ligands have also been identified for chemokine receptors. (tansobio.com)
- Many chemokine receptors function as HIV co-receptors, but CCR5 is the only one demonstrated to play an essential role in HIV/AIDS pathogenesis. (tansobio.com)
- Update on the extended family of chemokine receptors and introducing a new nomenclature for atypical chemokine receptors. (tansobio.com)
- the expression of chemokine receptors in different peripheral blood T-cell subsets in patients with polymyositis (PM) and dermatomyositis, was examined. (cusabio.com)
- Here we report that the chemokine receptor CCR10 is highly expressed in human glioblastoma compared with control brain tissue. (oncotarget.com)
- CCL27 binds specifically to chemokine receptor 10 (CCR10). (nih.gov)
- Reporter cells were transfected with either the expression plasmid for mouse chemokine (C-C motif) receptor 10 (Ccr10) or the mock plasmid and treated with various concentrations of the reference agonist. (tansobio.com)
- Most chemokines bind to more than one receptor subtype. (tansobio.com)
- The tables include both standard chemokine receptor names  and aliases. (tansobio.com)
- An atypical addition to the chemokine receptor nomenclature: IUPHAR Review 15. (tansobio.com)
- The herpesvirus 8-encoded chemokine vMIP-II, but not the poxvirus-encoded chemokine MC148, inhibits the CCR10 receptor. (ox.ac.uk)
- The viral chemokine antagonist vMIP-II encoded by human herpesvirus 8 (HHV8) and MC148 encoded by the poxvirus - Molluscum contagiosum - were tested against the newly identified chemokine receptor CCR10. (ox.ac.uk)
- High affinity receptor for the C-C type chemokines CCL17/TARC, CCL22/MDC and CKLF isoform 1/CKLF1. (cusabio.com)
- This gene encodes two isoforms of a receptor for monocyte chemoattractant protein-1, a chemokine which specifically mediates monocyte chemotaxis. (antikoerper-online.de)
- In vitro , signaling through CCL27-CCR10 mediates activation of p-Akt, and subsequently induces proliferation and invasive responses. (oncotarget.com)
- Cell proliferation and invasion promoted by CCL27 were blocked by inhibition of p-Akt or CCR10. (oncotarget.com)
- As the CCR10 ligand ESkine / CCL27 had the highest identity to MC148 and because both chemokines are expressed in the skin we suspected MC148 to block CCR10. (ox.ac.uk)
- CCL27 may also play a role in mediating homing of lymphocytes to cutaneous sites. (nih.gov)
- They also increase the expression of skin-associated chemokine CCL27 on keratinocytes, which stimulates the accumulation of cutaneous lymphocyte-associated antigen (CLA +) T-cell subsets to replace autoreactive (allergen-specific) CD4+ T-cell subsets. (lww.com)
- CCL27 is a member of the CC cytokine family, and is involved in immunoregulatory and inflammatory processes. (nih.gov)
- However, investigations in very early childhood examining immunological abnormalities such as altered neonatal cytokine/chemokine profiles in association with an aberrant developmental trajectory, are sparse. (nih.gov)
- Connexin26 (Cx26) plays an important role in ionizing radiation -induced damage, and CC chemokine ligand 27 (CCL27) regulates the skin immune response . (bvsalud.org)
- Proteins in the mitogen activated protein kinase (MAPK) signaling pathway and CCL27-related proteins were detected by immunoblotting . (bvsalud.org)
- A mouse model was established to examine the expression of CCL27 and skin inflammation in vivo. (bvsalud.org)
- Our findings show that Cx26 likely plays a role in the activation of the MAPK and NF-κB/COX-2 signaling pathways and regulates the secretion of CCL27 in keratinocytes after X-ray radiation -induced skin damage. (bvsalud.org)
- 8. The role of CCL21/CCR7 chemokine axis in breast cancer-induced lymphangiogenesis. (nih.gov)
- HaCaTCx26-/- cells were constructed to verify the effects of Cx26 on CCL27 secretion . (bvsalud.org)
- The secretion of CCL27 was significantly decreased in HaCaT wild-type cells relative to HaCaTCx26-/- cells . (bvsalud.org)
- IL-13 also induces secretion of chemokines that are required for recruitment of allergic effector cells to the lung. (wikidoc.org)
- Macrophage Inflammatory Protein MIP-1 alpha is part of the CC subfamily of the chemokine superfamily of chemoattractant cytokines. (creativebiomart.net)
- Chemokines in turn can be divided by structure into four subclasses by the number and arrangement of conserved cysteines. (tansobio.com)
- n = 17) and CX3C ( n = 1) chemokines all have four conserved cysteines, with zero, one and three amino acids separating the first two cysteines respectively. (tansobio.com)
- C chemokines ( n = 2) have only the second and fourth cysteines found in other chemokines. (tansobio.com)
- CCL27 functions as a chemotactic factor that attracts skin-associated memory T-lymphocytes. (nih.gov)
- 4. The CXCL12-CXCR4 chemokine pathway: a novel axis regulates lymphangiogenesis. (nih.gov)
- ... [read more] non-hematopoietic roles have been identified for many chemokines in the areas of embryonic development, immune cell proliferation, activation and death, viral infection, and as antibiotics, among others. (tansobio.com)
- 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)
- Zlotnik A, Yoshie O. Chemokines: a new classification system and their role in immunity. (tansobio.com)
- 13. Presence of circulating CCR10+ T cells and elevated serum CTACK/CCL27 in the early stage of mycosis fungoides. (nih.gov)
- 15. Cutting edge: the orphan chemokine receptor G protein-coupled receptor-2 (GPR-2, CCR10) binds the skin-associated chemokine CCL27 (CTACK/ALP/ILC). (nih.gov)
- 18. A possible role for CCL27/CTACK-CCR10 interaction in recruiting CD4 T cells to skin in human graft-versus-host disease. (nih.gov)
- CCL27 binds specifically to chemokine receptor 10 (CCR10). (nih.gov)
- 7. Identification of a novel chemokine (CCL28), which binds CCR10 (GPR2). (nih.gov)
- CCL27 functions as a chemotactic factor that attracts skin-associated memory T-lymphocytes. (nih.gov)
- 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)
- 3. CCL28 production in HaCaT cells was mediated by different signal pathways from CCL27. (nih.gov)