IL-18 (also known as IFN-gamma-inducing factor), although structurally unrelated to IL-12, shares with it the role of activating NK cells and polarizing T cells toward Th1 cell function. To understand how the IL-18 gene (and consequently Th1 function) is regulated, we have determined the gene structure and investigated the mechanisms of transcriptional control and cell type expression. The mouse IL-18 gene comprises seven exons distributed over 26 kb. Exons 1 and 2 of this gene are 5-noncoding exons. Promoter activity was detected upstream of these noncoding exons in two distinct regions. Both promoters are TATA-less and not G+C rich. The promoter activity located upstream of exon 2 was shown to act constitutively, while the activity located upstream of exon 1 was up-regulated in activated macrophage and T cell lines. IL-18 gene expression may be regulated in a wide range of cell types by the activities of these two distinct promoters. IL-18 is known to be synthesized as a precursor, pro-IL-18, and its
IL18 (IFN-gamma-inducing factor, IGIF) is a novel pro-inflammatory cytokine that augments natural killer (NK) activity in spleen cells.This cytokine…
IL18 - IL18 (untagged)-Human interleukin 18 (interferon-gamma-inducing factor) (IL18) available for purchase from OriGene - Your Gene Company.
Interpretation: Energy as a function of wavelength is a hyperbolic function. Notice that as wavelength decreases, the energy absorbed increases. For example, red light has wavelength of 680 nm and contains a considerable amount of energy, 42 kcal. However, a pigment molecule absorbing blue light, with a wavelength 400 nm, absorbs about 71 kcal of energy. Conclusions: The shorter the wavelength, the greater the energy absorbed. The different pigment molecules of plants absorb different wavelengths of light and consequently absorb different energies. Additionally, during photosynthesis, certain processes require higher energy than others. For example, photosystem II requires photons with slightly higher energies than photosystem I. As a result, chlorophyll molecules in photosystem II absorb light maximally at 680 nm while molecules in photosystem I can absorb light up to 700 nm.. Additional Questions:. 1. Ultraviolet light has a wavelength of 284 nm. Would you expect it to be more or less ...
Interleukin (IL)-37 has been known to play an immunosuppressive role in various inflammatory disorders, but whether it participates in the regulation of pathogenesis of adult-onset Stills disease (AOSD) has not been investigated. In this study, we examined serum IL-37 levels and their clinical association with AOSD, and we explored the anti-inflammatory effects of IL-37 on peripheral blood mononuclear cells (PBMCs) from patients with AOSD. Blood samples were collected from 62 patients with AOSD and 50 healthy control subjects (HC). The serum IL-37 levels were determined using an enzyme-linked immunosorbent assay (ELISA). The correlations of serum IL-37 levels with disease activity, laboratory values, and inflammatory cytokines in AOSD were analyzed by Spearmans correlation test. The correlations between serum IL-37 levels and clinical manifestations were analyzed by Mann-Whitney U test. PBMCs from ten patients with AOSD were stimulated with recombinant human IL-37 protein, and expression levels of
S100A8/A9 has been suggested as a marker of disease activity in patients with adult-onset Stills disease (AOSD). We evaluated the clinical significance of S100A8/A9 as a biomarker and its pathogenic role in AOSD. Blood samples were collected prospectively from 20 AOSD patients and 20 healthy controls (HCs). Furthermore, skin and lymph node biopsy specimens of AOSD patients were investigated for S100A8/A9 expression levels via immunohistochemistry. Peripheral blood mononuclear cells (PBMCs) of active AOSD patients and HCs were investigated for S100A8/A9 cell signals. S100A8/A9, interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) levels in active AOSD patients were higher than those of HCs. S100A8/A9 levels correlated positively with IL-1β, TNF-α and C-reactive protein. The inflammatory cells expressing S100A8/A9 were graded from one to three in skin and lymph node biopsies of AOSD patients. The grading for S100A8/A9 was more intense in the skin lesions with karyorrhexis, mucin deposition,
Adult-onset Stills disease (AOSD) is a systemic disorder characterized by intermittent fever, evanescent rash, arthralgias or arthritis and predominantly neutrophilic leucocytosis. We report on a 16-year-old woman with Stills disease who developed, in addition to the typical rash, persistent papular lesions on her face, neck and upper and lower back. Although the presence of fixed skin lesions is not a characteristic feature of AOSD, their appearance at the onset of the disease and their evolution suggest that they represent a specific manifestation of the disease.
A 39-year-old man with a 1-week history of fever, polyarthralgia, sore throat, and a salmon pink rash was admitted to our hospital. Laboratory findings based on blood samples, which were collected with ethylenediaminetetraacetic acid (EDTA) and counted 30 min after venipuncture, were as follows: white blood cell (WBC) count, 38,840/µL (neutrophils, 94.0%; eosinophils, 1.0%; monocytes, 1.0%; lymphocytes, 1.0%; basophils, 0.8%; metamyelocytes, 2.2%); red blood cell (RBC) count, 4.19×106/µL; hemoglobin level, 12.1 g/dL; platelet count, 138×103/µL; immunoglobulin (Ig)G, 1.050 g/dL; IgM, 0.184 g/dL; IgA, 0.264 g/dL; and C-reactive protein, 25.3 mg/dL. The antinuclear antibody titer was 1:40. The ferritin level was 953.5 ng/mL (normal range, 5-157 ng/mL). Finally, the patient was diagnosed with adult-onset Stills disease (AOSD). On day 5 after admission, the patient was treated with prednisolone (PSL, 40 mg/day) and subsequently with PSL in combination with tacrolimus (TAC, 2 mg/day). On the day ...
Care guide for Adult-onset Stills Disease (Ambulatory Care). Includes: possible causes, signs and symptoms, standard treatment options and means of care and support.
Journal of the American Academy of Dermatology - Vol. 58 - N° 3 - p. 533-535 - Iconography : Adult-onset Stills disease revealed by facial edema - EM|consulte
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The arthralgias had started six weeks prior to his new admission. The joint pain had started in his left wrist. It then spread to the knees, ankles, hips and shoulders. The pain did not worsen with activity and was not relieved by rest. The patient reported he had noticed progressive hand swelling. His pain had worsened to the point that walking was unbearable. He reported fever, loss of appetite, nausea and vomiting. He also reported having had one or two extremely watery, mucous-laden stools just prior to his emergency department visit.. On admission, the patient was noted to have numerous laboratory abnormalities: hyponatremia with a sodium level of 130 mEq/L (reference range [RR]: 136-145); hypokalemia with potassium at 3.0 mEq/L (RR: 3.5-5.1); a chloride level of 92 mEq/L (RR: 98-107); hypocalcemia with a level of 7.9 mg/dL (RR: 8.5-10.1); aspartate amino-transferase of 109 units/L (RR: 15-37); alanine aminotransferase of 84 units/L (RR: 12-78); elevated alkaline phosphatase of 158 units/L ...
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A 32-year-old woman presented in 1991 with a 2-month history of fever reaching 39.5°C and associated with arthritis in the knees, ankles and shoulders, a nonpruritic skin rash, myalgia and weight loss. Her laboratory studies, including liver function tests, were within the normal ranges except that she had an elevated erythrocyte sedimentation rate (ESR) of 110 mm/hr and lactate dehydrogenase (LDH) of 1975 IU/L (Normal Range: 200-480). The rheumatoid factor and antinuclear antibodies were negative. Blood cultures were also negative. On physical examination she was found to have several enlarged right anterior cervical lymph nodes (2 × 3 cm in size) and left posterior auricular lymph nodes (0.5 × 1 cm in size) all of which were non-tender, immobile and rubbery. In addition, she had swelling in both knee joints and ankle joints. Papular skin lesions on the neck and upper abdomen were evident. No hepatosplenomegaly was detected. A chest radiograph revealed pleural effusion in the left lower lung ...
Dr. George Still first described Stills Disease in 1897. It is a form of juvenile rheumatoid arthritis that has systemic features. Although it is more commonly found in children, the disorder can be present in adults, where it is known as Adult-Onset Stills Disease. The cause is unknown, but a common symptom of Stills Disease is intermittent high fevers. Salmon-colored skin rash that does not itch is also common. Other physical symptoms include joint pain, fatigue and sore throat. The heart, lungs, spleen and lymph glands may become inflamed. Diagnosis is difficult because the symptoms often resemble those of other types of arthritis. Diagnosis is made after careful physical examination, medical history, blood tests and x-rays. Source: ArthritisInsight.com Originally published by The Tribune-Review. (c) 2008 Tribune-Review/Pittsburgh Tribune-Review. Provided by ProQuest LLC. All rights Reserved.. ...
Fever is a prominent feature of AOSD (incidence 95.7%-100%) and frequently presents as hyperpyrexia (≥ 39°C)2,3,4,5,6,7,8. In our study, hyperpyrexia (≥ 39°C) was noted in 66 patients with AOSD (94.29%) and displayed a NPV of 92.86% with a NLR of 0.15, indicating that a diagnosis of AOSD is unlikely in patients without hyperpyrexia. However, fever is also the common symptom for tumors and infections. A previous study20 reported only slight fever in elderly patients with AOSD. Caution must be exercised to exclude AOSD if the patient has unexplained fever. Therefore patients with fever were selected as the control group in our series.. In our series, rash, arthralgia, and sore throat1,16,18,21 were more sensitive (, 70%) and specific (, 70%), with a PLR of 3.29-4.86, suggesting that these 3 features are helpful for establishing a diagnosis of AOSD. The NLR of the 3 features was lower (0.26-0.32), indicating their value in ruling out AOSD based on the absence of these features. Actually, ...
Plasma interleukin-38 in patients with rheumatoid arthritis. Int Immunopharmacol. 2018 Sep 26;65:1-7 Authors: Xu WD, Su LC, He CS, Huang AF Abstract Previous studies have indicated that interleukin-38 (IL-38) is involved in rheumatoid arthritis (RA). The present study aims to assess plasma levels of IL-38 in RA and discuss the potential of IL-38 as a biomarker for RA. Protein...
Results. Serum levels of cell-free DNA, myeloperoxidase (MPO)-DNA complex, and α-defensin were significantly increased in patients with AOSD compared to HC. Serum levels of the NET molecules, cell-free DNA, MPO-DNA, and α-defensin were correlated with several disease activity markers for AOSD. In followup of patients with AOSD after treatment with corticosteroid, the levels of cell-free DNA and α-defensin decreased significantly. On immunohistochemistry, neutrophil elastase-positive and MPO-positive inflammatory cells were detected in skin and LN of patients with AOSD, and were expressed in fiber form in the lesions. The serum from patients with active AOSD induced NETosis in neutrophils from HC. NET molecules induced interleukin 1β production in monocytes, representing a novel mechanism in the pathogenesis of AOSD. ...
ASC is an adaptor protein which contains two protein-protein interaction domains; N-terminal - pyrin domain (PYC) and C-terminal - caspase recruitment domain (CARD).. ASC plays an important role in inflammation and apoptosis. It is a component of several inflammatory complexes, inflammasomes, which are important for caspase-1 activation, processing and secretion of pro-inflammatory cytokines (IL-1β, IL-18). It promotes pyropoptosis in macrophages and induces caspase-mediated apoptosis (involving caspase-8 and caspase-9).. Additionally, ASC is involved in transcriptional control of cytokine and chemokine expression independent of the inflammasome.. ...
Interleukin-18 (bahasa Inggris: interleukin-18, interferon-gamma-inducing factor, IL-18) adalah sitokina yang merupakan ekspresi genetik IL18,[1] dengan prekursor sepanjang 192 AA dan protein aktif sepanjang 157 AA yang meningkatkan respon peradangan tubuh dengan menginduksi sekresi interferon-gamma oleh sel T dan meningkatkan aktivitas sel NK di dalam limpa. IL-18 umumnya merupakan sekresi makrofaga dan sel Kupffer.[2] Peningkatan ekspresi IL-18 ditemukan pada beberapa jenis kanker, adenomiosis,[3] dan Hashimoto tiroiditis.[4] ...
Rare: Neutropenia, thrombocytopenia. Drug Interactions: Concurrent use of other immunosuppressants, particularly TNF antagonists, may increase risk of infection. Patient Instructions: Avoid live virus vaccines. Avoid pregnancy. Stop injections if an infection or a fever develops that lasts more than a few days.. Comments: Combination therapy with methorexate is generally well tolerated and is more effective than monotherapy. Anakinra appears less effective than TNF antagonists and other modern drugs for RA and is little used for RA in clinical practice. Combination with TNF antagonists is avoided because of increased risk of infection. In case-series, anakinra treatment for 3 days (off-label) is effective for the treatment of acute gout in patients unable to tolerate, or not responding to, standard therapies such as NSAIDs, colchicine or corticosteroids. In small case-series, anakinra has also been reported to be effective in other conditions including adult-onset Stills disease and idiopathic ...
Accelerated increase in serum interleukin-1 receptor antagonist (IL-1Ra) starts 6 years before diagnosis of type 2 diabetes: Whitehall II prospective cohort ...
Inflammasomes are large protein complexes formed in response to cellular stresses that are platforms for recruitment and activation of caspase 1
To the Editor. We read the article of Osuka et al. (1) entitled A Protective Role for Inflammasome Activation Following Injury with great interest. However, we are concerned that the authors have not sufficiently ruled out the possibility that the major effects attributed to inflammasome inhibition were merely due to the solvent used.. The authors describe inflammasome activation in burned mice 1 day after injury as revealed by caspase 1 activation and increased interleukin 1β (IL-1β) production. Interestingly, the data suggest that inhibiting caspase 1 activity-and thereby inhibiting inflammasome activation-with the Ac-YVAD-cmk peptide did not reduce inflammation as expected. On the contrary, it caused a significantly higher mortality and increased expression of the proinflammatory cytokines IL-6 and IL-33 as compared with untreated burned mice. The authors therefore conclude that inflammasome activation might have a protective role following severe injury. Inhibition of (pro)caspase 1 ...
Inflammatory responses play a key role in many neural pathologies, with localized signaling from the non-immune cells making critical contributions. The NLRP3 inflammasome is an important component of innate immune signaling and can link neural insult to chronic inflammation. The NLRP3 inflammasome requires two stages to contribute: priming and activation. The priming stage involves upregulation of inflammasome components while the activation stage results in the assembly and activation of the inflammasome complex. The priming step can be rate limiting and can connect insult to chronic inflammation, but our knowledge of the signals that regulate NLRP3 inflammasome priming in sterile inflammation is limited. This study examined the link between mechanical strain and inflammasome priming in neural systems. Transient non-ischemic elevation of intraocular pressure (IOP) increased mRNA for inflammasome components IL-1β, NLRP3, ASC and CASP1 in rat and mouse retinas. The elevation was greater one day after
There is a clear need for interdisciplinary research and publications that bring together scientists who work on the inflammasome. This protein complex, termed the inflammasome and many of its components are implicated in disease disorders, autoimmune and infectious diseases. The structure, activation and regulation of the inflammasome complex have been and are still studied in increasing number of laboratories around the world. Our goal is to provide an issue summarizing every fascinating aspect of inflammasome activation and modulation of the innate immune response to microbial and to danger signals. This issue will bring the experts in inflammasome research up to speed with the most recent findings. However, several reviews are geared towards introducing the new scientists to the inflammasome complex and to the fundamental and essential information that will help them understand and even pursue their studies in this direction. By looking at the two sides of the coin, notably, some authors focused on
Associates of the mammalian nucleotide holding domains, leucine-rich do it again (LRR)-containing receptor family members of protein are essential modulators of innate defenses controlling irritation. the existence of ROS inhibitors as NAC, or DPI. Astonishingly, SK-N-MC cells perform not really react to ATP enjoyment in spite of G2A7Ur reflection. These outcomes offer a system by which risk indicators and particulate matter mediate irritation via the inflammasome in the lack of microbial an infection. Launch Inflammasomes are multiprotein processes accountable for the account activation of caspase-1, and caspase-5 proteases needed for account activation and digesting of proinflammatory cytokines IL-1 and IL-18 [1], [2]. To time, four bonafide inflammasomes called by the PRR that adjusts their activity possess been discovered: the NALP1, NALP3, AIM2 and NLRC4 inflammasomes. With the exemption of Purpose2, the various other inflammasomes include a PRR that is supposed to be to the Nod-like ...
TY - JOUR. T1 - Surge of serum interleukin-2 level in a Japanese patient with cytarabine syndrome. AU - Iida, Yasunori. AU - Yasudo, Hiroki. AU - Fukano, Reiji. AU - Azuma, Yoshihiro. AU - Ichimura, Takuya. AU - Ohga, Shouichi. AU - Hasegawa, Shunji. PY - 2020/3/1. Y1 - 2020/3/1. UR - http://www.scopus.com/inward/record.url?scp=85076929700&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=85076929700&partnerID=8YFLogxK. U2 - 10.1002/pbc.28131. DO - 10.1002/pbc.28131. M3 - Letter. C2 - 31850653. AN - SCOPUS:85076929700. VL - 67. JO - Pediatric Blood and Cancer. JF - Pediatric Blood and Cancer. SN - 1545-5009. IS - 3. M1 - e28131. ER - ...
From Science Daily, implications for why vocal tone is so influential, either in song or in speech: A new study in the journal PLoS ONE finds that people use the same brain regions to produce and understand intonation in speech. Many studies suggest that people learn by imitating through so-called mirror neurons. This study shows…
Background: Inflammatory responses play a key role in the pathophysiology of myocardial ischemia-reperfusion (I/R) injury. ASC is an adaptor protein that forms inflammasome whose activation leads to caspase-1-dependent interleukin (IL)-1β generation and subsequent inflammatory responses; however, the role of ASC in myocardial I/R injury remains to be determined.. Methods and Results: ASC deficient (ASC−/−) and wild-type (WT) mice were subjected to 30 min LAD occlusion, followed by reperfusion. ASC−/− mice showed improved LV dysfunction (%FS: 34.0% vs. 25.7% at 14 days p,0.01), reduced infarct area/area at risk (IA/AAR: 18.7% vs. 28.6% at 48 h, p,0.01), and scar formation (scar/LV area: 9.7% vs. 14.6% at 14 days, p,0.01) after myocardial I/R. Immunostaining revealed decreased infiltration of macrophages (Mac3) and neutrophils (Gr-1), but not neovascularization (CD31), in the injured myocardium of the ASC−/− mice. Real-time RT-PCR and ELISA analyses demonstrated that the myocardial ...
ICD-10 Code: M06.1. Definition: AOSD is a systemic inflammatory disease that typically afflicts young adults. It is characterized by quotidian fevers, evanescent rashes, and chronic polyarthritis.. Etiology: The cause of AOSD is unknown. AOSD is the adult continuum of systemic juvenile arthritis (SoJIA) and likely shares a common etiology. Both the adult and juvenile Stills disease exhibit the same manifestations, clinical course and response to treatment. However, adults are more likely to complain of a prodromal sore throat, without proof of infection. Hence, because of the febrile onset and sore throat, AOSD has infrequently been associated with a variety of viral infections, including rubella, Epstein-Barr virus, Coxsackie B4, and mumps, although no single agent has been proven to inciting or pathogenic. AOSD appears to be an autoinflammatory syndrome as it shares many of the features seen in these inflammasome activation disorders reflecting a disorder of the inate immune response with ...
Adult onset of Stills disease (AOSD) is a rare systemic inflammatory disease. Cardiorespiratory complications are mainly represented by pleural and pericardial disorders and are less frequent than cutaneous and articular complaints. Pulmonary arterial hypertension (PAH) occurring in AOSD is rarely described in literature. We present the case of a young patient who developed severe PAH 2 years after diagnosis of AOSD. This is a rare and severe complication which is probably underestimated. PAH in AOSD can be lethal, and unfortunately its occurrence is unpredictable. Echocardiographic screening of AOSD patients should be evaluated in further trials. Currently, the most suitable treatment is still unknown.
Within the last decade numerous advances have already been manufactured in the part and regulation of inflammasomes during pathogenic and sterile insults. to a number of pathogenic and physiological stimuli. Inflammasome activation can be an essential element of the innate immune system response and is crucial for the clearance of pathogens or broken cells. Nevertheless overt inflammasome activation can be a major drivers of autoimmune and metabolic disorders root the need for understanding this technique in physiological and pathological contexts. The inflammasome detectors are grouped relating with their structural features into nucleotide-binding domain-like receptors (NLRs) absent in melanoma 2-like receptors (ALRs) as well as the lately identified pyrin. The power is got by These receptors to put together inflammasomes and activate the cysteine protease caspase-1. As well as the sensor (NLR ALR or pyrin) and enzymatic element (caspase-1) most inflammasomes also make use of an adaptor ...
We thank Vendrame and Dotta (1) for their interesting perspective regarding our recently published study investigating the role of interleukin-16 (IL-16) in the development of insulitis and type 1 diabetes in female NOD mice (2). On the basis of previous studies correlating suboptimal activation of caspase-3 with the development of autoimmunity in the clinical setting (3,4), they propose a similar condition might exist in NOD mice, resulting in defective secretion of mature IL-16. Although we have not directly examined this possibility, it must be considered that many studies have wrestled with the difficulty in detecting secreted IL-16 in several mouse strains used to examine inflammatory responses (2,5). This likely reflects the biology of mature IL-16, which is active at concentrations as low as 10−11 M, and indicates that the low levels of intrapancreatic mature IL-16 detected during the development of insulitis is not restricted only to the NOD genetic background.. However, the notion ...
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February 13, 2018. The assembly of the NLRP3 inflammasome can promote the release of IL-1β/IL-18 and initiate pyroptosis. Accordingly, the dysregulation of NLRP3 inflammasome activation is involved in a variety of... ...
Inflammasome activation is associated with numerous diseases. However, in vivo detection of the activated inflammasome complex has been limited by a dearth of tools. We developed transgenic mice that ectopically express the fluorescent adaptor protein, ASC (apoptosis-associated speck-like protein containing a caspase recruitment domain), and characterized the formation of assembled inflammasome complexes (specks) in primary cells and tissues. In addition to hematopoietic cells, we found that a stromal population in the lung tissues forms specks during the early phase of influenza infection whereas myeloid cells showed speck formation after two days. In a peritonitis and Group B streptococcus infection models, a higher percentage of neutrophils formed specks at early phases of infection, while dendritic cells formed specks at later time points. Furthermore, speck-forming cells underwent pyroptosis, and extensive release of specks to the extracellular milieu in vivo. These data underscore the ...
The results presented in this study show that inflammasome formation and IL-1β processing is induced by hyperoxia in vivo and in vitro and is associated with increased alveolar epithelial protein permeability. Hyperoxia-stimulated K+ efflux, inflammasome formation, proinflammatory cytokine release, and marked induction of caspase-1 and IL-1β cleavage. The P2X7 agonist ATP enhanced hyperoxia-induced inflammasome activation, whereas the P2X7 antagonist, oxATP, inhibited hyperoxia-induced inflammasome activation. However, when ATP was scavenged with apyrase, hyperoxia-induced inflammasome activation was significantly decreased, indicating the possible involvement of the P2X7 receptor. Furthermore, shRNA silencing of inflammasome component expression abrogated hyperoxia-induced secretion of proinflammatory cytokines in vitro. These results suggest that hyperoxia induces K+ efflux through the P2X7 receptor and leads to inflammasome activation and secretion of proinflammatory cytokines.. Our studies ...
PYCARD, often referred to as ASC (Apoptosis-associated speck-like protein containing a CARD), is a protein that in humans is encoded by the PYCARD gene. It is localized mainly in the nucleus of monocytes and macrophages. In case of pathogen infection, however, it relocalizes rapidly to the cytoplasm, perinuclear space, endoplasmic reticulum and mitochondria and it is a key adaptor protein in activation of the inflammasome . NMR structure of full-length ASC: PDB ID 2KN6 [1] This gene encodes an adaptor protein that is composed of two protein-protein interaction domains: a N-terminal PYRIN-PAAD-DAPIN domain (PYD) and a C-terminal caspase-recruitment domain (CARD). The PYD and CARD domains are members of the six-helix bundle death domain-fold superfamily that mediates assembly of large signaling complexes in the inflammatory and apoptotic signaling pathways via the activation of caspase. In normal cells, this protein is localized to the cytoplasm; however, in cells undergoing apoptosis, it forms ...
Exaggerated inflammasome activation in venous thrombosis in CD39-deficient mice. Extracellular release of ATP and ADP through cell death, injury, or activation is a potent stress response, altering the local microenvironment to activate paracrine and autocrine signaling pathways (18, 19). Binding of extracellular ATP to the plasma membrane receptor ionophore P2X7 activates a potent stress-response-signaling pathway characterized by potassium efflux, which triggers assembly and activity of the inflammasome, a multiprotein oligomer that activates highly proinflammatory cytokines including IL-1β (20). Gupta et al. recently reported increased NLRP3 inflammasome assembly in patients at high altitude at risk for DVT (21). Canonical inflammasome activation requires a priming step marked by NF-κB activation and inflammasome component transcription (20). A second signal initiates NLRP3-mediated assembly and oligomerization of inflammasome component fibers, proteolytic cleavage of pro-caspase-1 to ...
Jen, H.-Y., Chuang, Y.-H., Lin, S.-C., Chiang, B.-L. and Yang, Y.-H. (2011), Increased serum interleukin-17 and peripheral Th17 cells in children with acute Henoch-Schönlein purpura. Pediatric Allergy and Immunology, 22: 862-868. doi: 10.1111/j.1399-3038.2011.01198.x ...
Standard Inflammasomes Signaling Antibodies from AdipoGen Life Sciences. All AdipoGen products are supplied by Bio-Connect, the benelux distributor.
Pyroptosis is a form of lytic programmed cell death initiated by inflammasomes, which detect cytosolic contamination or perturbation. This drives activation of caspase-1 or caspase-11/4/5, which cleave gasdermin D, separating its N-terminal pore-forming domain (PFD) from the C-terminal repressor dom …
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Important Note: The ABC compiler includes a module system inspired by my Open Modules proposal (Ongkingco et al., AOSD 06). However, this implementation does not enforce the critical property of Open Modules: that clients will not be affected by semantics-preserving changes to the implementation of a module. In order to obtain this property, it is important that clients of a module only advise exposed join points through named pointcuts in the module interface. External aspects must never refer to internal join points except through those names. I mention this here because the difference has led to some to think that Open Modules does not enforce this property ...
有多种机制认为病毒感染与过敏性炎症相互作用,从而导致下呼吸道功能障碍、喘息和哮喘。首先,潜在的过敏性炎症可以直接增强气道对鼻病毒感染的反应性。此外,病毒感染可损害气道上皮的屏障功能,导致气道壁对气传过敏原的吸收增加和炎症反应增强,而潜在的过敏性炎症也可能导致病毒复制增强。值得注意的是,鼻病毒感染和变应原均可促进气道上皮细胞产生IL-33, IL-33是最近发现的一种先天细胞因子,可促进2型气道炎症和重塑。据报道,这种类固醇耐药途径在难以控制哮喘的儿童中上调。有趣的是,IL-33多聚物与中晚期发作的喘息有关,而中晚期发作的喘息与早期生活中的过敏反应密切相关。 另一种先天上皮细胞因子IL-25也由鼻病毒诱导,在过敏患者鼻病毒感染的情况下,IL-25可能加重过敏性气道炎症 ...
Инфламмасома - важный компонент нативного иммунитета. Она представляет собой макромолекулярный комплекс, включающий сенсорные элементы, адапторные белки и зимоген каспазы-1. Под действием продуктов распада тканей и патогенных микроорганизмов инфламмасома активируется и превращает про-IL-1b и про-IL-18 в активные интерлейкины. Активация инфламмасом отмечена при многих воспалительных заболеваниях и служит мишенью для терапевтических воздействий. В настоящем обзоре обсуждается вклад инфламмасом в патогенез социально-значимых заболеваний ...
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