The purpose of this study was to investigate the lesions of a mouse collagen antibody-induced arthritis (CAIA) model using fluorescence bioimaging and micro-computed tomography (micro-CT) and to compare it with histopathological examination. Twelve mice were randomly divided into three groups: group 1 (G1) as control, group 2 (G2) as fluorescence probe control and group 3 (G3) as collagen antibody-induced arthritis. The mice of G3 intravenously received anti-type II collagen 5-clone antibody cocktail (2 mg/mouse) on day 0 and intraperitoneally received lipopolysaccharide (|TEX|$50{\mu}g/mouse$|/TEX|) on day 3. On the while, the mice of G1 and G2 received 0.9% saline in equal volumes at equivalent times. Fluorescence bioimaging and micro-CT analysis were carried out to assess arthritis. Treatment with the collagen antibody cocktail increased the paw thickness of mice compared to those in both the control and probe-treated groups. Fluorescence bioimaging using a near infrared imaging agent showed high

Les Produits de Chondrex Modèles animaux Anticorps Tests danticorps Recherche sur les bactéries Recherche contre le cancer Collagène Collagénase HMGB1 Dosages de protéines Coloration des tissus Tampons dimmunoanalyse Métabolisme cellulaire Les MSDS ou fiches de données de sécurités Protocoles Gentaur Assay kits en collaboration Animal Model Protocols Arthritis Scoring System Collagen Antibody-Induced Arthritis - Mouse (cat# 53010, 53040, 53100) Collagen-Induced Arthritis - Mouse Collagen-Induced Arthritis - Mouse (Visual Guide) Collagen-Induced Arthritis - Rat Adjuvant-Induced Arthritis - […]. ...

Studies in IL-6-deficient (IL-6-/-) mice highlight that IL-6 contributes to arthritis progression. However, the molecular mechanism controlling its activity in vivo remains unclear. Using an experimental arthritis model in IL-6-/- mice, we have established a critical role for the soluble IL-6R in joint inflammation. Although intra-articular administration of IL-6 itself was insufficient to reconstitute arthritis within these mice, a soluble IL-6R-IL-6 fusion protein (HYPER-IL-6) restored disease activity. Histopathological assessment of joint sections demonstrated that HYPER-IL-6 increased arthritis severity and controlled intrasynovial mononuclear leukocyte recruitment through the CC-chemokine CCL2. Activation of synovial fibroblasts by soluble IL-6R and IL-6 emphasized that these cells may represent the source of CCL2 in vivo. Specific blockade of soluble IL-6R signaling in wild-type mice using soluble gp130 ameliorated disease. Consequently, soluble IL-6R-mediated signaling represents a ...

The Rho family GTPase Rac1 regulates cytoskeletal rearrangements crucial for the recruitment, extravasation and activation of leukocytes at sites of inflammation. Rac1 signaling also promotes the activation and survival of lymphocytes and osteoclasts. Therefore, we assessed the ability of a cell-permeable Rac1 carboxy-terminal inhibitory peptide to modulate disease in mice with collagen-induced arthritis (CIA). CIA was induced in DBA/1 mice, and in either early or chronic disease, mice were treated three times per week by intraperitoneal injection with control peptide or Rac1 inhibitory peptide. Effects on disease progression were assessed by measurement of paw swelling. Inflammation and joint destruction were examined by histology and radiology. Serum levels of anti-collagen type II antibodies were measured by enzyme-linked immunosorbent assay. T-cell phenotypes and activation were assessed by fluorescence-activated cell sorting analysis. Results were analyzed using Mann-Whitney U and unpaired Student

Methods Expression levels of Mincle mRNA was determined in inflamed paws from hTNFtg and IL1-/-IL6-/-hTNFtg mice by qPCR. To study the role of mincle deficiency in experimental arthritis, we generated mincle-/-hTNFtg mice as well as their hTNFtg littermates. Mice were weekly assessed for clinical signs of arthritis from week 4 to 11 after birth. We quantitatively analysed inflammatory joint destruction in H&E, TRAP and TB stained sections from hind paws. The effect of mincledeficiency was also evaluated in the K/BxN serum transfer model. Therefore, mincle-/- and mincle+/+ mice received i.v. injections of K/BxN serum on day 1 and day 3. Animals were assessed from day1 to 12 for clinical signs of arthritis. Quantitative histopathological analysis were performed as above mentioned in hind paws.. ...

TY - JOUR. T1 - Inhibition of Notch signalling ameliorates experimental inflammatory arthritis. AU - Park, Jong Sung. AU - Kim, Seol Hee. AU - Kim, Kwang Meyung. AU - Jin, Cheng Hao. AU - Choi, Ki Young. AU - Jang, Jiyeon. AU - Choi, Yuri. AU - Gwon, A. Ryeong. AU - Baik, Sang Ha. AU - Yun, Ui Jeong. AU - Chae, Su Young. AU - Lee, Seulki. AU - Kang, Young Mo. AU - Lee, Kang Choon. AU - Arumugam, Thiruma V.. AU - Mattson, Mark P.. AU - Park, Jae Hyung. AU - Jo, Dong Gyu. PY - 2015/1/1. Y1 - 2015/1/1. N2 - Objective: To test the hypothesis that Notch signalling plays a role in the pathogenesis of rheumatoid arthritis (RA) and to determine whether pharmacological inhibition of Notch signalling with γ-secretase inhibitors can ameliorate the RA disease process in an animal model.Methods Collagen-induced arthritis was induced in C57BL/6 or Notch antisense transgenic mice by immunisation with chicken type II collagen (CII). C57BL/6 mice were administered with different doses of inhibitors of ...

The use of regulatory or immature dendritic cells (DCs) as tools for modulating experimental rheumatoid arthritis is very recent. TNF-stimulated DCs have been shown to restore tolerance in experimental autoimmune encephalomyelitis and collagen-induced arthritis (CIA).. Objective: We investigated the capacity of short-term lipopolysaccharide (LPS)-stimulated DCs pulsed with type-II collagen (CII) to induce tolerance against established CIA.. Methods: Bone marrow-derived DCs were generated in the presence of GM-CSF. After CIA induction, mice were injected at day 35 with a single dose of 4- or 24-hour LPS-stimulated DCs that had been loaded with CII (CII/DCs, 4hLPS/CII/DCs or 24hLPS/CII/DCs). Arthritis progression was monitored by clinical and histologic evaluations.. Results Flow cytometry of 4hLPS/CII/DCs showed intermediate CD40 and CD86 expression, lower than that of 24hLPS/CII/DCs (fully mature) and higher than that of CII/DCs (immature). A functional assay showed that 4hLPS/CII/DCs display ...

Experimental Arthritis: ARTHRITIS that is induced in experimental animals. Immunological methods and infectious agents can be used to develop experimental arthritis models. These methods include injections of stimulators of the immune response, such as an adjuvant (ADJUVANTS, IMMUNOLOGIC) or COLLAGEN.

Most antirheumatic therapies are given systemically, which may result in complications because of the high dosage needed to achieve therapeutic levels in the joints. Gene therapy might provide a more efficient system to deliver therapeutic compounds at the site of inflammation. The artificial chromosome expression system (ACes) is a unique, nonintegrating, nonviral gene-expression system, which functions like a natural chromosome. This technology offers advantages over current expression systems because it allows stable expression of genes producing single or multiple proteins over long periods. We are developing ex vivo gene therapy using artificial chromosomes containing reporter genes (LacZ or RFP) for local delivery of genes in rats with adjuvant arthritis. The aim of this study was to evaluate the transfection efficiency in cell lines or primary cells, including rat skin fibroblasts (RSFs) and fibroblast-like synoviocytes (FLSs). Furthermore, we investigated the feasibility of local ...

There is considerable evidence implicating tumor necrosis factor alpha (TNF-alpha) in the pathogenesis of rheumatoid arthritis. This evidence is based not only on the universal presence of TNF-alpha in arthritic joints accompanied by the upregulation of TNF-alpha receptors but also on the effects of neutralizing TNF-alpha in joint cell cultures. Thus, neutralization of TNF-alpha in vitro results in inhibition of the production of interleukin 1, which like TNF-alpha, is believed to contribute to joint inflammation and erosion. To determine the validity of this concept in vivo, the effect of administering TNF-neutralizing antibodies to mice with collagen-induced arthritis has been studied. This disease model was chosen because of its many immunological and pathological similarities to human rheumatoid arthritis. TN3-19.12, a hamster IgG1 monoclonal antibody to murine TNF-alpha/beta, was injected i.p. into mice either before the onset of arthritis or after the establishment of clinical disease. Anti-TNF

It has been demonstrated that pterostilbene inhibits reactive oxygen species production in neutrophils in vitro. However, little is known about its effects on neutrophils during inflammation in vivo. In this study, the effect of pterostilbene on neutrophil activity was investigated in experimental arthritis model. Lewis rats were injected by a single intradermal injection of heat-killed Mycobacterium butyricum in Freunds adjuvant to develop arthritis. Another group of arthritic animals received pterostilbene 30mg/kg, daily, p.o. The number and activity of neutrophils in blood were measured on a weekly basis during the whole experiment. Moreover, the total radical trapping potential in plasma was measured at the end of the experiment. In the pterostilbene treated arthritic group, the treatment significantly lowered the number of neutrophils in blood on days 14 and 21 without significant downregulation of neutrophil oxidative burst. Pterostilbene nonsignificantly increased total radical trapping ...

A rapid and synchronized alternative to the CIA and K/BxN models that reduces variability, eliminates the need for expensive colonies and conserves test compound, controls and vivarium space.

Incidence and severity of K/BxN serum transfer-induced arthritis are not reduced in IL-36 receptor (R) knockout (KO) mice. Incidence of arthritis (A), arthritis

Fingerprint Dive into the research topics of Transforming growth factor β-transduced mesenchymal stem cells ameliorate experimental autoimmune arthritis through reciprocal regulation of Treg/Th17 cells and osteoclastogenesis. Together they form a unique fingerprint. ...

DIAS, Renata Gonçalves; SAMPAIO, Sandra Coccuzzo; SANTANNA, Morena Brazil; et al. Articular inflammation induced by an enzymatically-inactive Lys49 phospholipase A2: activation of endogenous phospholipases contributes to the pronociceptive effect. Journal of Venomous Animals and Toxins including Tropical Diseases, London, v. 23, p. 13 , 2017. Disponível em: < http://dx.doi.org/10.1186/s40409-017-0104-0 > DOI: 10.1186/s40409-017-0104-0 ...

In humans and in animal models, susceptibility to arthritis is under complex genetic control, reflecting influences on the immunological processes that initiate autoimmunity and on subsequent inflammatory mechanisms in the joints. The effector phases are conveniently modeled by the K/BxN serum transfer system, a robust model well suited for genetic analysis where arthritis is initiated by pathogenic Ig. Here, we mapped the genetic loci distinguishing the high-responder BALB/c vs. low-responder SJL strains. After computational modeling of potential breeding schemes, we adapted a stepwise selective breeding strategy, with a whole-genome scan performed on a limited number of animals. Several genomic regions proved significantly associated with high sensitivity to arthritis. One of these regions, on distal chr2, was centered on the interleukin 1 gene family. Quantitation of transcripts of the Il1a and Il1b candidate genes revealed a 10-fold greater induction of Il1b mRNA in BALB/c than in SJL

The DNA binding activity of AP-1 and NF-kappaB are markedly increased in both CIA and RA. In CIA, activation of AP-1 and NF-kappaB precede both clinical arthritis and metalloproteinase gene expression. NF-kappaB expression correlated better than AP-1 with metalloproteinase expression.

Second, in order to investigate whether other MHC genes also contribute to arthritis susceptibility, we assessed arthritis development in congenic strains mapped to other parts of the MHC region. We identified a second arthritis-regulatory QTL in the MHC class III region, that regulates not only the onset and severity, but also chronicity of arthritis. We subsequently mapped this effect to a conserved, 33-kb large haplotype Ltab-Ncr3 comprising five polymorphic genes. Interestingly, unlike other positionally-identified arthritis genes in rats, Ltab-Ncr3 regulates only adjuvant arthritis models but not autoimmunity triggered by specific tissue antigens, such as type II collagen. Furthermore, we found that gene expression and alternative splicing of the Ltab-Ncr3 genes correlate remarkably with arthritis severity and some of the gene expression differences were reproduced in a cohort of RA patients and healthy controls ...

PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

Peptide analogues of disease-associated epitopes were studied for inhibition of experimental allergic encephalomyelitis (EAE) and adjuvant arthritis (AA) in Lewis rats. EAE- and AA-associated analogues were selected as competitors because of their in vitro inhibitory activity on proliferation of encephalitogenic and arthritogenic T cells. Although the EAE-associated competitor had a superior major histocompatibility complex (MHC) binding affinity, the AA-associated competitor was a better inhibitor of the in vitro proliferation of arthritogenic T cells. Furthermore, although in vivo EAE was inhibited by both competitors, AA was only inhibited by the AA-associated competitor. Remarkably, in contrast to what was expected of a regular MHC competitor peptide, the AA-associated peptide analogue also prevented AA upon immunization before disease induction and appeared to induce T cell responses that crossreacted with the original disease-associated epitope. Therefore, it is concluded that ...

In collagen-induced arthritis (CIA) of mouse, self-reactive T cells recognize a peptide antigen from type II collagen (CII). CII is of particular interest, as an autoimmune response to this protein leads to CIA in mice, rats, and primates. Activation of T cells is believed to be an important pathogenic factor in autoimmune disease. So, T cells have become a focal point of study for the development of novel therapeutic approaches to the treatment of autoimmune disease. In this study, we evaluated the efficacy and mechanism of recombinant MHC II molecules in regulation of the antigen-specific T cell clones by using mouse I-Aq, combined with an auto-antigen peptide from type II collagen (CII260-274) in CIA model. It was found that recombinant I-Aq/CII260-274 molecules not only activate CII-specific T cell clone but also inhibit the same clone in vitro according to the condition of stimulation. Furthermore, development of CIA in mice was successfully prevented by the in vivo injection of a ...

Celastrol exhibits anti-arthritic effect in rheumatoid arthritis (RA), but the role of celastrol-mediated Ca mobilization in treatment of RA remains unelucidated. Here, we illustrate the regulatory role of celastrol-induced Ca signalling in synovial fibroblasts of RA patients and adjuvant-induced arthritis (AIA) in rats. Molecular target of celastrol was determined by computational docking, Ca dynamic and functional assays on SERCA. Ca -mediated autophagy in RASFs/RAFLS and the underlying mechanism were verified by quantification of endogenous LC3-II puncta, immunoblotting, and flow cytometry with the Ca chelator (BAPTA/AM) or suitable inhibitors. The anti-arthritic effect of celastrol, autophagy induction and growth rate of synovial fibroblasts in AIA rats were monitored by microCT and immunofluorescence staining. mRNA from joint tissues of AIA rats was isolated for transcriptional analysis of inflammatory genes. The role of Ca in regulating the identified genes was investigated by knockdown of ...

Celastrol exhibits anti-arthritic effect in rheumatoid arthritis (RA), but the role of celastrol-mediated Ca mobilization in treatment of RA remains unelucidated. Here, we illustrate the regulatory role of celastrol-induced Ca signalling in synovial fibroblasts of RA patients and adjuvant-induced arthritis (AIA) in rats. Molecular target of celastrol was determined by computational docking, Ca dynamic and functional assays on SERCA. Ca -mediated autophagy in RASFs/RAFLS and the underlying mechanism were verified by quantification of endogenous LC3-II puncta, immunoblotting, and flow cytometry with the Ca chelator (BAPTA/AM) or suitable inhibitors. The anti-arthritic effect of celastrol, autophagy induction and growth rate of synovial fibroblasts in AIA rats were monitored by microCT and immunofluorescence staining. mRNA from joint tissues of AIA rats was isolated for transcriptional analysis of inflammatory genes. The role of Ca in regulating the identified genes was investigated by knockdown of ...

Abs to the α-chain of the IL-2 receptor (anti-CD25) are used clinically to achieve immunosuppression. Here we investigated the effects of DNA vaccination with the whole CD25 gene on the induction of rat adjuvant arthritis. The DNA vaccine protected the rats and led to a shift in the cytokine profile of T cells responding to disease target antigens from Th1 to Th2. The mechanism of protection was found to involve the induction of an antiergotypic response, rather than the induction of anti-CD25 Abs. Antiergotypic T cells respond to activation molecules, ergotopes, expressed on syngeneic activated, but not resting, T cells. CD25-derived peptides function as ergotopes that can be recognized by the antiergotypic T cells. Antiergotypic T cells taken from control sick rats did not proliferate against activated T cells and secreted mainly IFN-γ. In contrast, antiergotypic cells from CD25-DNA-protected rats proliferated against activated T cells and secreted mainly IL-10. Protective antiergotypic T ...

Animals, Antibodies; Monoclonal/pharmacology, Antigen-Antibody Complex/immunology, Arthritis; Experimental/genetics/*immunology, Collagen Type II/immunology, Comparative Study, Genetic Predisposition to Disease, Immunoglobulin G/*metabolism, Macrophages; Peritoneal/*immunology, Mice, Mice; Mutant Strains, Receptors; IgG/antagonists & inhibitors/genetics/*metabolism, Research Support; Non-U.S. Govt ...

Rhomboid family member 2 gene (Rhbdf2) is an inactive homologue lacking essential catalytic residues of rhomboid intramembrane serine proteases. The protein is necessary for maturation of tumor necrosis factor-alpha (TNF-α) converting enzyme, which is the molecule responsible for the release of TNF-α. In this study, Rhbdf2 knockout (KO) mice were produced by CRISPR/CAS9. To see the effects of the failure of TNF-α release induced by Rhbdf2 gene KO, collagen-induced arthritis (CIA), which is the representative TNF-α related disease, was induced in the Rhbdf2 mutant mouse using chicken collagen type II. The severity of the CIA was measured by traditional clinical scores and histopathological analysis of hind limb joints. A rota-rod test and grip strength test were employed to evaluate the severity of CIA based on losses of physical functions. The results indicated that Rhbdf2 mutant mice showed clear alleviation of the clinical severity of CIA as demonstrated by the significantly lower severity ...

A risk score encompassing clinical characteristics, serologic findings, and imaging tests could be used to predict which antibody-positive patients are likely to go on to develop rheumatoid arthritis,

Destruction of cartilage and bone is a poorly managed hallmark of human rheumatoid arthritis (RA). p38 Mitogen-activated protein kinase (MAPK) has been shown to regulate key proinflammatory pathways in RA, including tumor necrosis factor α, interleukin (IL)-1β, and cyclooxygenase-2, as well as the process of osteoclast differentiation. Therefore, we evaluated whether a p38α MAPK inhibitor, indole-5-carboxamide (SD-282), could modulate cartilage and bone destruction in a mouse model of RA induced with bovine type II collagen [collagen-induced arthritis (CIA)]. In mice with early disease, SD-282 treatment significantly improved clinical severity scores, reduced bone and cartilage loss, and reduced mRNA levels of proinflammatory genes in paw tissue, including IL-1β, IL-6, and cyclooxygenase-2. Notably, SD-282 treatment of mice with advanced disease resulted in significant improvement in clinical severity scoring and paw swelling, a reversal in bone and cartilage destruction as assessed by ...

Mediators of Inflammation is a peer-reviewed, Open Access journal that publishes original research and review articles on all types of inflammatory mediators, including cytokines, histamine, bradykinin, prostaglandins, leukotrienes, PAF, biological response modifiers and the family of cell adhesion-promoting molecules.

These findings raise the important question of why TNFα blockade is effective in reducing disease activity despite increasing numbers of Th1 and Th17 cells. To address this question, we used an adoptive transfer system established previously (15) to confirm that the expanded Th1/Th17 cells were potentially pathogenic. Spleen and LN cells from arthritic mice treated for 10-14 d with anti-TNFα mAb or control Ab were pooled and injected into CB-17 SCID mice (5 × 107 cells/mouse or 107 cells/mouse). The SCID recipients were also injected i.p. with 100 μg of type II collagen without adjuvant, which is required for the successful transfer of arthritis (15). The proportion of LN cells to spleen cells was ∼1:10 and was identical in both anti-TNFα-treated and control groups.. Transfer of 5 × 107 cells from either anti-TNFα-treated or control mice led to efficient transfer of arthritis, although onset of arthritis was much earlier when donor cells were derived from anti-TNFα-treated mice (Fig. ...

Find anti inflammatory antiarthritic effects. Mississsippi Stem Cell Therapy Center promotes stem cell therapy and regenerative medicine.

Immune and inflammatory systems are controlled by multiple cytokines, including ILs and INFs. These cytokines exert their biological functions through Janus tyrosine kinases and STAT transcription factors. One such cytokine, IL-6, has been proposed to contribute to the development of rheumatoid arthritis (RA). We found that STAT3 was strongly tyrosine phosphorylated in synovial tissue of RA patients, but not those with osteoarthritis. Blockade of the IL-6-gp130-JAK-STAT3-signaling pathway might therefore be beneficial in the treatment of RA. We show here that the mRNA for the endogenous cytokine signaling repressor CIS3/SOCS3 is abundantly expressed in RA patients. To determine whether CIS3 is effective in treating experimental arthritis, a recombinant adenovirus carrying the CIS3 cDNA was injected periarticularly into the ankle joints of mice with antigen-induced arthritis or collagen-induced arthritis (CIA). Periarticular injection of CIS3 adenovirus drastically reduced the severity of ...

The 60 kDa heat shock protein (HSP60) has been reported to influence T-cell responses in two ways: as a ligand of toll-like receptor 2 signalling and as an antigen. Here we describe a new mechanism of T-cell immuno-regulation focused on HSP60: HSP60 is up-regulated and presented by activated T cells (HSP60 is an ergotope) to regulatory (anti-ergotypic) T cells. Presentation of HSP60 by activated T cells was found to be MHC-restricted and dependent on accessory molecules - CD28, CD80 and CD86. Anti-ergotypic T cells responded to T-cell HSP60 by proliferation and secreted IFNγ and TGFβ1. In vitro, the anti-ergotypic T cells inhibited IFNγ production by their activated T-cell targets. In vivo, adoptive transfer of an anti-ergotypic HSP60-specific T-cell line led to decreased secretion of IFNγ by arthritogenic T cells and ameliorated adjuvant arthritis (AA). Thus, the presentation of HSP60 by activated T cells turns them into targets for anti-ergotypic regulatory T cells specific for HSP60. ...

(a)-(c) Typical histological appearance of CIA mouse paws: (a) severe inflammatory cellular infiltration-synovitis and pannus formation; (b) bone and cartil

Aggravation of Cold-Restraint Stress-Induced Gastric Lesions in Adjuvant Arthritic Rats : Pathogenic Role of Inducible and Endothelial Nitric Oxide （2009 ...

BioAssay record AID 184149 submitted by ChEMBL: Inhibition of streptococcal cell wall-washed arthritis model in rats at 30.0 mg/kg peroral dose.

Rheumatoid arthritis (RA) is characterized by progressive inflammation of the synovial joints that leads to the breakdown of cartilage and bone …

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PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.

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TY - JOUR. T1 - Effective treatment of established murine collagen-induced arthritis by systemic administration of dendritic cells genetically modified to express IL-4. AU - Kim, S. H.. AU - Kim, S.. AU - Evans, C. H.. AU - Ghivizzani, S. C.. AU - Oligino, T.. AU - Robbins, P. D.. N1 - Copyright: Copyright 2017 Elsevier B.V., All rights reserved.. PY - 2001/3/1. Y1 - 2001/3/1. N2 - Dendritic cells (DC) are APCs that are able to stimulate or inhibit immune responses, depending on levels of expression of MHC class I and II costimulatory molecules and cytokines. Our previous studies have suggested that the observed contralateral effect, where injection of a vector carrying certain immunomodulatory genes into one joint resulted in inhibition of arthritis in untreated joints, is mediated by in vivo modification of DC. Therefore, we have examined the ability of genetically modified DC to suppress established murine collagen-induced arthritis (CIA) after i.v. delivery. IL-4 has been shown to partially ...

TY - JOUR. T1 - Successful gene therapy via intraarticular injection of adenovirus vector containing CTLA4IgG in a murine model of type II collagen-induced arthritis. AU - Ijima, K.. AU - Murakami, M.. AU - Okamoto, H.. AU - Inobe, M.. AU - Chikuma, S.. AU - Saito, I.. AU - Kanegae, Y.. AU - Kawaguchi, Y.. AU - Kitabatake, A.. AU - Uede, T.. PY - 2001/8/9. Y1 - 2001/8/9. N2 - We previously constructed an adenovirus vector carrying a gene encoding a soluble form of fusion protein, consisting of the extracellular portion of cytotoxic lymphocyte antigen 4 (CTLA4) and the Fc portion of human immunoglobulin G1 (Adex1CACTLA4IgG). Murine type II collagen-induced arthritis (CIA) was treated with Adex1CACTLA4IgG. A single intraarticular injection of 1 × 105 PFU was able to support serum CTLA4IgG at more than 10 μg/ml for at least 12 weeks and was able to inhibit the CIA clinically and histo-logically. In contrast, intravenous, intramuscular, or subcutaneous injection of 1 × 105 PFU was unable to ...

Abstract: To evaluate the effect of methotrexate on collagen-induced arthritis, micro-computed tomography (micro-CT) and histopathological analyses were used in male Wistar rats. Rats were divided randomly into three groups. Group 1 was treated with 0.9% saline, and groups 2 and 3 were boosted with type Ⅱ collagen. From day 21 to 42, groups 1 and 2 were orally treated with 0.9% saline and group 3 was orally treated with 1.5 mg/kg methotrexate. All rats were sacrificed at day 42 after the first collagen treatment. Micro-CT analyses showed bony parameters, such as bone volume and trabecular number, were decreased in group 2 compared to group 1, and these parameters were recovered in group 3. Histopathological examination and pathological parameter scoring showed that the knee joints of rats in group 2 had severe joint destruction, showing cartilage and bone erosion, enlarged cavities with inflammatory cell infiltration and activation of synovial fibroblasts. By contrast, these changes were ...

TY - JOUR. T1 - Anti-inflammatory effects of licorice and roasted licorice extracts on TPA-induced acute inflammation and collagen-induced arthritis in mice. AU - Chung, Won Yoon. AU - Kim, Ki Rim. AU - Jeong, Chan Kwon. AU - Park, Kwang Kyun. AU - Choi, Jong Hoon. AU - Park, Jung Han Yoon. AU - Lim, Soon Sung. PY - 2010/5/6. Y1 - 2010/5/6. N2 - The anti-inflammatory activity of licorice (LE) and roated licorice (rLE) extracts determined in the murine phorbol ester-induced acute inflammation model and collagen-induced arthritis (CIA) model of human rheumatoid arthritis. rLE possessed greater activity than LE in inhibiting phorbol ester-induced ear edema. Oral administration of LE or rLE reduced clinical arthritis score, paw swelling, and histopathological changes in a murine CIA. LE and rLE decreased the levels of proinflammatory cytokines in serum and matrix metalloproteinase-3 expression in the joints. Cell proliferation and cytokine secretion in response to type II collagen or ...

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Genome-wide association studies have identified various susceptibility variants and loci associated with incidence of rheumatoid arthritis (RA) in different populations. One of these is T cell activation Rho GTPase activating protein (TAGAP). The present study sought to measure the expression of TAGAP in RA patients, CD4(+) T cells subsets from healthy humans and in mice with collagen-induced arthritis. Peripheral blood mononuclear cells (PBMC) from RA patients and tissues of arthritic mice at different stages of the disease were used for the evaluation of TAGAP mRNA expression. Increased TAGAP expression was observed in RA patients compared to healthy controls, and there were differences in the expression level of TAGAP in the tissues of mice with experimental arthritis. Gene expression in CD4(+) T cells from healthy humans was greatest 4 h after activation and protein expression was greatest after 24 h. The expression of TAGAP was not correlated with CD4(+) lymphocyte subsets which were enriched for

ASCs also promoted Treg generation in peripheral tissues, including dLNs, peritoneum, synovium, and peripheral blood. MSCs (ASCs) on in vitro formation of bone-resorbing osteoclasts and pathological bone loss in the mouse collagen-induced arthritis (CIA) model of RA. We observed that ASCs significantly inhibited receptor activator of NF-B ligand (RANKL)Cinduced osteoclastogenesis in both AMG 487 a contact-dependent and -independent manner. Additionally, ASCs inhibited RANKL-induced osteoclastogenesis in the presence of proinflammatory cytokines such as TNF-, IL-17, and IL-1. Furthermore, treatment with ASCs at the onset of CIA significantly reduced clinical symptoms and joint pathology. Interestingly, ASCs protected periarticular and systemic bone loss in CIA mice by maintaining trabecular bone structure. We further observed that treatment with ASCs reduced osteoclast precursors in bone marrow, resulting in decreased osteoclastogenesis. Moreover, ASCs suppressed autoimmune T cell responses and ...

OBJECTIVE: Endothelins (ETs) are involved in several inflammatory events. The present study investigated the efficacy of bosentan, a dual ETA/ETB receptor antagonist, in collagen-induced arthritis (CIA) in mice. TREATMENT: CIA was induced in DBA/1J mice. Arthritic mice were treated with bosentan (100 mg/kg) once a day, starting from the day when arthritis was clinically detectable. METHODS: CIA progression was assessed by measurements of visual clinical score, paw swelling and hypernociception. Histological changes, neutrophil infiltration and pro-inflammatory cytokines were evaluated in the joints. Gene expression in the lymph nodes of arthritic mice was evaluated by microarray technology. PreproET-1 mRNA expression in the lymph nodes of mice and in peripheral blood mononuclear cells (PBMCs) was evaluated by real-time PCR. The differences were evaluated by one-way ANOVA or Students t test. RESULTS: Oral treatment with bosentan markedly ameliorated the clinical aspects of CIA (visual clinical score,

TY - JOUR. T1 - Intra-articular injection of hyaluronate and indomethacin in rabbits with antigen-induced arthritis. AU - Lo, Yow Jen. AU - Sheu, Ming Thau. AU - Tsai, Wen Chi. AU - Lin, Yun Ho. AU - Li, Jau Le. AU - Liang, Yu Chih. AU - Chang, Chi Ching. AU - Hsieh, Ming-Shium. AU - Chen, Chien Ho. PY - 2007/10. Y1 - 2007/10. N2 - Combined effects of hyaluronate and indomethacin in the treatment of rabbits with antigen-induced arthritis (AIA) were evaluated by assessing joint swelling, C-reactive protein (CRP) and prostaglandin E2 (PGE 2) levels with periodic intra-articular (ia) injections of hyaluronate alone (HA group) and with either a low or high concentration of indomethacin (LI-HA or HI-HA group). End-point analyses included matrix metalloproteinases-3 (MMP-3) activity and macroscopic and histological joint examinations. Results demonstrated that treatment in LI-HA and HI-HA groups resulted in statistically significant suppression of CRP, PGE2, and MMP-3 in comparison with those of HA ...

Mast cells are abundantly expressed in synovial tissues and have been proposed to exert proinflammatory effects primarily based on antibody transfer-induced disease models (28, 29). The mode of mast cell activation and the mechanism by which activated-mast cells mediate antigen-induced arthritis are largely unknown and likely complex. We now provide direct in vivo evidence that IL-33 plays a major role in mast cell activation in the context of antigen-induced arthritis. Thus, IL-33 enhanced CIA when ST2−/− mice were reconstituted with BMMCs from WT but not from ST2−/− mice (Fig. 5). Our data also provide mechanisms by which mast cells could promote inflammatory synovitis (Fig. 6). IL-33 induces mast cell production of IL-1, IL-6, IL-13, and a range of chemokines (13, 14, 30) (Fig. 4). Because both IL-1 and IL-6 play crucial roles in the induction of Th17 cells (31-33), a key pathogenic cell type in arthritis (21, 22), our studies indicate a relationship between ST2/IL-33 function and ...

IL-17 is implicated in the pathogenesis of rheumatoid arthritis (RA) and has previously been shown to be induced by tumor necrosis factor (TNF) in vitro. The aim of this study was to assess the impact of TNF inhibition on IL-17 production in collagen-induced arthritis, a model of RA. TNF blockade using TNFR-Fc fusion protein or anti-TNF monoclonal antibody reduced arthritis severity but, unexpectedly, expanded populations of Th1 and Th17 cells, which were shown by adoptive transfer to be pathogenic. Th1 and Th17 cell populations were also expanded in collagen-immunized TNFR p55(-/-) but not p75(-/-) mice. The expression of IL-12/IL-23 p40 was up-regulated in lymph nodes (LN) from p55(-/-) mice, and the expansion of Th1/Th17 cells was abrogated by blockade of p40. Treatment of macrophages with rTNF also inhibited p40 production in vitro. These findings indicate that at least one of the ways in which TNF regulates Th1/Th17 responses in arthritis is by down-regulating the expression of p40. Finally,

Nimesulide is a COX-2 inhibitor used for symptomatic relief of rheumatoid arthritis. Leflunomide is an anti-pyrimidine used to manage the progression of rheumatoid arthritis. Herein we studied the influence of nimesulide and leflunomide combination in terms of disease symptoms and progression using collagen-induced arthritis model in mice, as a model for rheumatoid arthritis. Collagen induced arthritis was induced by immunization with type II collagen. Assessment of joint stiffness and articular hyperalgesia were evaluated using a locomotor activity cage and the Hargreaves method, respectively. Disease progression was assessed via arthritic index scoring, X-ray imaging, myeloperoxidase enzyme activity and histopathologic examination. Nimesulide induced only transient symptomatic alleviation on the top of decreased leucocytic infiltration compared to arthritis group. However, nimesulide alone failed to induce any significant improvement in the radiological or pathological disease progression. Leflunomide

Rheumatoid arthritis (RA) is a systemic autoimmune disease mediated by T cells. Collagen type II (CII) is one of the autoantigens associated with RA. CII263-272 is a predominant CII antigenic peptide that can induce T-cell activation upon binding to MHC and interaction with the appropriate T-cell receptor (TCR). Altered CII263-272 peptides with substitution of specific amino acids could bind to RA-associated HLA-DR4/1 with no T cell stimulating effects and could inhibit T cell activation in RA. We performed this study to evaluate the effect of mucosal administration and to explore the mechanism of the inhibitory effect of altered CII263-272 peptide (267Q --> A, 270K --> A and 271G --> A) on collagen induced arthritis (CIA). CIA was induced in Lewis rats by immunization with bovine CII. Altered CII263-272 peptide was given intranasally beginning from arthritis onset. Wild CII263-272 peptide or PBS was administered as controls. Therapeutic effects were evaluated by arthritis scores, body weight ...

TY - JOUR. T1 - Collagen-induced arthritis and TCRs in SWR and B10.Q mice expressing an E(α)/(k) transgene. AU - Griffiths, M. M.. AU - Nabozny, G. H.. AU - Hanson, J.. AU - Harper, D. S.. AU - McCall, S.. AU - Moder, K. G.. AU - Cannon, G. W.. AU - Luthra, H. S.. AU - David, C. S.. PY - 1994. Y1 - 1994. N2 - B10.E(α)/(k) transgenic mice were mated with H2-E- B10.Q and SWR mice. F1 and F1 x parental strain backcross progeny were tested for arthritis and autoimmune reactivity to mouse type II collagen (MII) after immunization with bovine, chick, deer, or human type II collagen. The results were correlated with the H-2 haplotype (b/q vs q/q) and the TCR Vβ profile of peripheral blood T cells in each mouse. Hybrid progeny expressed TCR profiles different from either parent because of the TCR Vβ genomic deletions of SWR mice (Vβa), the wild-type TCR allele of C57Bl/10 (B10) mice (Vβb), and the intrathymic negative selection processes resulting from cell surface expression of ...

Recently, therapy with bone marrow mesenchymal stem cells (BMMSCs) has been attempted to relieve rheumatoid arthritis (RA) and reconstruct cartilage injury. However, treatment has been unsuccessful in complete prevention of persistent cartilage destruction and resulted in inferior outcomes of cartilage regeneration. Scaffolds are an important construct in the field of cartilage tissue engineering, but their role in arthritis treatment has not yet been fully examined. Here, we transplanted two types of scaffold-assisted BMMSCs: fibrin gel- and poly(l-lactide-co-glycolide)−poly(ethylene glycol)−poly(l-lactide-co-glycolide) (PLGA−PEG−PLGA) hydrogel-assisted BMMSCs referred as FGB and HGB groups, respectively, into subchondral defects for the treatment of antigen-induced arthritis. The administration of exogenous BMMSCs ameliorated joint swelling and decreased both joint surface temperature and inflammatory cytokine levels in both groups. Immune cell composition of the inflammation of surrounding

Objectives: To establish if changes in Th1/Th17 cell populations previously reported in experimental arthritis occur in patients with rheumatoid arthritis (RA) treated with anti-tumour necrosis factor α (TNFα) agents, and whether the therapeutic response to anti-TNFα is compromised in patients and mice because of elevated Th17/IL-17 levels. Finally, to assess the efficacy of combined blockade of anti-TNFα and anti-IL-17 in experimental arthritis. Methods: A longitudinal study of two independent cohorts (cohort 1, n=24; cohort 2, n=19) of patients with RA treated with anti-TNFα biological agents was carried out to assess their Th17/IL-17 levels before and after the start of anti-TNFá therapy. IL-12/23p40 production was assessed in plasma Peripheral blood lymphocytes (PBLs) and monocytes. Mice with collagen-induced arthritis (CIA) were treated with anti-TNFα alone, anti-IL17 alone or a combination of the two. Efficacy of treatment and response was assessed from changes in Disease Activity Score 28

In countries where parasitic infections are endemic, autoimmune disease is relatively rare, leading to the hypothesis that parasite-derived immunomodulators may protect against its development. Consistent with this, we have previously demonstrated that ES-62, a 62 kDa phosphorylcholine (PC)-containing glycoprotein that is secreted by filarial nematodes, can exert anti-inflammatory action in the murine collagen-induced arthritis (CIA) model and human rheumatoid arthritis-derived synovial tissue cultures. As a first step to developing ES-62-based drugs, the aim of this study was to determine whether the PC-moiety of ES-62 was responsible for its anti-inflammatory actions. We compared the anti-inflammatory activity of a PC-free form of recombinant ES-62 (rES-62) and a synthetic PC-ovalbumin conjugate (OVA-PC) with that of native ES-62 in the CIA model and synovial tissues from patients with rheumatoid arthritis. Results: The anti-inflammatory actions of ES-62 in CIA appear to be dependent on the PC ...

article{418b5550-2321-4395-ab0c-946f90945ceb, abstract = {OBJECTIVE: To characterize the arthritis-modulating effects of 3 non-major histocompatibility complex (MHC) quantitative trait loci (QTLs) in rat experimental arthritis in the disease-resistant E3 strain, and to investigate the disease-modulating effects of the MHC region (RT1) in various genetic backgrounds. METHODS: A congenic fragment containing Ncf1 along with congenic fragments containing the strongest remaining loci, Pia5/Cia3 and Pia7/Cia13 on chromosome 4, were transferred from the arthritis-susceptible DA strain into the background of the completely resistant E3 strain. The arthritis-regulatory potential of the transferred alleles was evaluated by comparing the susceptibility to experimental arthritis in congenic rats with that in E3 rats. The RT1(u) haplotype from the E3 strain was transferred into the susceptible DA strain (RT1(av1)), and various F(1) and F(2) hybrids were generated to assess the effects of RT1 on arthritis ...

Background A long-term existing schistosome infection can certainly help in keeping immuno-homeostasis, thus providing protection against various types of autoimmune diseases to the infected sponsor. human rheumatoid arthritis. Illness by Schistosoma japonicum significantly reduced the severity and the incidence of experimental autoimmune collagen-induced arthritis. However, this beneficial effect can only be provided by a pre-established acute stage of illness but not by a pre-established early stage of the illness. The safety against collagen-induced arthritis correlated with reduced levels of anti-collagen II IgG, especially the subclass of IgG2a. Moreover, in safeguarded mice increased levels of IL-4 were present at the time of collagen II injection together with sustained higher IL-4 levels during the course of arthritis development. In contrast, in unprotected mice minimal levels of IL-4 were ITF2357 present at the initial stage of collagen II challenge together with lack of IL-4 induction ...

METHODS: Female wistar (Ws) rats were used in this study. CIA was induced by Native bovine type II collagen emulsified with complete Freunds adjuvant (CFA). Beta-END was administered i.p. to CIA rats every other day from the 14th day (secondary immunization) to the 35th day after primary immunization. Clinical assessments were performed by two independent, blinded examiners every other day. Pathological and radiological observations were taken on the 35th day after the primary immunization. Tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), interleukin-6 (IL-6), regulated upon activation, normal T-cell expressed and secreted (RANTES), inducible NO syntheses (iNOS), matrix metalloproteinase-2 (MMP-2) and MMP-9 mRNA expression of synovium tissues of CIA rats was estimated by quantitative RT-PCR. The frequency of spleen Th1 and Th2 cells were assessed by fluorescence activated cell sorter (FACS) assay ...

Introduction: The Vbeta12-transgenic mouse was previously generated to investigate the role of antigen-specific T cells in collagen-induced arthritis (CIA), an animal model for rheumatoid arthritis. This mouse expresses a transgenic collagen type II (CII)-specific T-cell receptor (TCR) beta-chain and consequently displays an increased immunity to CII and increased susceptibility to CIA. However, while the transgenic Vbeta12 chain recombines with endogenous alpha-chains, the frequency and distribution of CII-specific T cells in the Vbeta12-transgenic mouse has not been determined. The aim of the present report was to establish a system enabling identification of CII-specific T cells in the Vbeta12-transgenic mouse in order to determine to what extent the transgenic expression of the CII-specific beta-chain would skew the response towards the immunodominant galactosylated T-cell epitope and to use this system to monitor these cells throughout development of CIA. Methods: We have generated and ...

Human Rheumatoid Arthritis powerpoint presentation slides is available for free download uploaded in belonging ppt presentation Health & Wellness category, Download and Use!

TY - JOUR. T1 - Myeloid DAP12-associating lectin (MDL)-1 regulates synovial inflammation and bone erosion associated with autoimmune arthritis. AU - Joyce-Shaikh, Barbara. AU - Bigler, Michael E.. AU - Chao, Cheng Chi. AU - Murphy, Erin E.. AU - Blumenschein, Wendy M.. AU - Adamopoulos, Iannis. AU - Heyworth, Paul G.. AU - Antonenko, Svetlana. AU - Bowman, Edward P.. AU - McClanahan, Terrill K.. AU - Phillips, Joseph H.. AU - Cua, Daniel J.. PY - 2010/3/15. Y1 - 2010/3/15. N2 - DNAX adaptor protein 12 (DAP12) is a trans-membrane adaptor molecule that transduces activating signals in NK and myeloid cells. Absence of functional Dap12 results in osteoclast defects and bone abnormalities. Because DAP12 has no extracelluar binding domains, it must pair with cell surface receptors for signal transduction. There are at least 15 known DAP12-associating cell surface receptors with distinct temporal and cell type-specific expression patterns. Our aim was to determine which receptors may be important in ...

B cells have a central role in the pathogenesis of collagen-induced arthritis (CIA), an animal model of the autoimmune disease rheumatoid arthritis. In this report, a specific subset of an innate type of B cells, B-1 B cells, have been studied for the involvement in CIA. The B-1 B cells were shown to produce small amounts of collagen-specific antibodies upon stimulation in vitro, suggesting that they play a minor role in the development of CIA. This report also includes how marginal zone B cells, another innate type of B cells with natural collagen-reactivity, can be identified in the medullary sinuses of lymph nodes of collagen-immunized mice, implying involvement in auto antigen trapping. ...

Y-320 is an orally active immunomodulator, and inhibits IL-17 production by CD4 T cells stimulated with IL-15 with IC50 of 20 to 60 nM. Y-320 also inhibits the production of IFN-γ and TNF-α by mouse CD4 T cells stimulated with IL-15, CXCL12, and anti-CD3 mAb. Y-320 (0.3-3 mg/kg p.o.) ameliorates collagen-induced arthritis (CIA) in Mice with a reduction of IL-17 mRNA in arthritic joints, and also shows therapeutic effects on CIA in cynomolgus monkeys. Moreover, Y-320 shows a synergistic effect in combination with anti-TNF-α mAb on chronic-progressing CIA in mice. Selleck Chemicals Y-320, IL-17 Inhibitor. 26 Sep 2014. Ushio H, et al. (2013). A new phenylpyrazoleanilide, y-320, inhibits interleukin 17 production and ameliorates collagen-induced arthritis in mice and cynomolgus monkeys. Pharmaceuticals (Basel). 7 (1): 1-17. doi:10.3390/ph7010001. PMC 3915191 . PMID 24366113 ...

Therapeutic Treatment of Arthritic Mice with 15-Deoxy Δ12,14-Prostaglandin J2 15d-PGJ2 Ameliorates Disease through the Suppression of Th17 Cells and the Induction of CD4 CD25−FOXP3 Cells. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.

Rheumatoid arthritis progression has been markedly improved by the application of biological anti-RA agents, which suppress RA activity and also repair affected joint space under certain conditions.

Elevated expression of LL-37 and its activating protease have been described in RA patients (6, 64), and mechanistic studies are beginning to unravel the role of LL-37 in this disease. Periarticular osteopenia is a common finding among patients with RA (65), and LL-37 induces apoptosis of osteoblasts, which could contribute to reduced bone formation in arthritic joints (7). Furthermore, a recent report characterized elevated expression of LL-37 primarily in the osteoclasts and granulocytes within the human RA synovium (66). Using a pristane-induced arthritis model in rats, upregulation of rCRAMP, the rat ortholog of LL-37, was demonstrated in granulocytes, macrophages, and γδ T cells of synovial fluid. Importantly, transfer of pristane-exposed neutrophils induced arthritis, whereas type I IFN or autoantibody responses in control rats did not (66). This suggests that LL-37 may contribute to arthritis development, but further studies are needed to clarify its role.. An association between ...

Phasic changes in the immune response were observed in rats and mice with adjuvant disease: stimulation of antibody formation on the seventh day after injection of Freunds complete adjuvant (FCA)...

Doctors use the rheumatoid arthritis severity scale to track the level and progress of your disease. Find out what it measures and what your numbers mean.

We have now previously reported a rise in interleukin (IL)-oneβ and IL-17 amounts, along with a ongoing activation of caspase-1 in early rheumatoid arthritis (RA) patients. These success recommend that medications concentrating on IL-1β regulatory pathways, Together with tumor necrosis variable (TNF), may perhaps constitute promising therapeutic agents in early RA. We have just lately utilized a THP-one macrophage-like mobile line to screen 2320 compounds for those who down-regulate both of those IL-1β and TNF secretion. Celastrol was one of the most promising therapeutic candidates determined in that review. Our major aim within the existing get the job done was to research no matter whether administration of celastrol can attenuate inflammation in a very rat design of adjuvant-induced arthritis (AIA). Additionally, since IL-1β is thought to Perform a task within the polarization of Th17 cells, we also investigate irrespective of whether administration of digoxin, a specific inhibitor of ...

The application of tumor necrosis factor inhibitors (TNFi) is a major breakthrough in the treatment of rheumatoid arthritis (RA). While the anti-inflammatory nature of TNFi is thought to contribute to the therapeutic effects, recent data show that the pharmacology of TNF- blockade is probably...

The arthritis-susceptible DA rat is one of the most commonly used rat strains for genetic linkage analysis and is instrumental for the identification of many genetic loci. Even though DA rats were kept as inbred lines at different institutes and suppliers, it became obvious that the various breeding …

Background The systems underlying tolerance maintenance and induction in autoimmune arthritis stay elusive. to na?ve rodents ameliorated the advancement of CII-induced joint disease. Bottom line Our data recommend that endogenous display of the CII-peptide on N cells can be one of the essential members to joint disease patience induction and maintenance. Electronic ancillary materials The online edition of this content (doi:10.1186/s13075-016-1037-7) contains supplementary materials, which is obtainable to authorized users. IgG ELISA Heat-killed L37Ra (Difco,?BD Biosciences,?Franklin Ponds, New Shirt,?USA) 0.4?mg/ml was dissolved in carbonate barrier, and filtered through a 22?m Millipore filtration system. A 96-well dish (Nunc Maxisorp) was covered with 100?d per good of the option and incubated in 4?C further and overnight blocked with PBS with BSA 1?%, Tween 1?%. The serum was serially diluted from 1:8 to 1:512 and the dish was incubated at 4?C overnight. Biotinylated goat anti-mouse IgG ...

Stem cell-derived tissue- associated regulatory T cells ameliorate the development of autoimmune arthritis. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.

OBJECTIVE: We studied histological changes in the cell populations of subchondral bone marrow resulting from inflammation in animal models of arthritis. Inflammation in intraosseous spaces and the effect of treatment with the aminobisphosphonate zoledronate were assessed. METHODS: Peripheral blood, femoral bone marrow, and spleen cells were harvested from carrageenan-induced arthritis Sprague-Dawley rats; fluorescence stained for CD3, CD8, CD4, CD11b/c, anti-mononuclear phagocyte (MNP), CD3/CD8, CD3/CD4, and MNP/CD11b/c; and evaluated by flow cytometry. Arthritis was induced in New Zealand white rabbits in 5 treatment groups: normal, arthritis, zoledronate-treated from arthritis induction, or 2 or 4 weeks after induction. Animals were euthanized after 7 weeks and distal femoral condyles were decalcified, processed, sectioned, and stained. Sections were evaluated for several cell types and histological features relevant to inflammation, which were assigned a categorical grade from 0 (healthy ...

Delayed type hypersensitivity. On Day 1 of the study, mice were IV injected with washed sheep red blood cells (SRBC). On Day 6 of the study, mice were treated with either vehicle or Dexamethasone followed by injection of SRBCs into the paws. Injection of SRBCs into the paws of sensitized mice produced an allergic reaction as measured by swelling (paw thickness). Dexamethasone, a steroid anti-inflammatory, significantly reduced footpad swelling as measured using a microcaliper. Data are mean ± SEM; ***p,0.001 compared to vehicle (N=7-8).. The mouse DTH model is a test against an immunological inflammatory response. Animals that received vehicle treatment displayed an increased paw thickness compared to animals administered Dexamethasone, providing an immunological benefit. These data demonstrate a valid methodology for producing an allergic reaction in experimental animals and show that these animals are sensitive to pharmacological agents that are known to reduce allergic reactions.. ...

The other day I was talking with my aunt about her severe arthritis. She kept mentioning that her hands and knees were really bothering her and no matter what she tried, she could get no relief.

University of Melbourne researchers have identified a protein involved in rheumatoid arthritis-induced inflammation that could lead to new drug treatments.

The importance of the BCR and TLR9 in autoimmunity and in the production of autoantibodies is well established but the underlying molecular mechanism still needs to be determined. Here we aim to characterize the BCR-TLR9 crosstalk by its effect on T-bet, as T-bet is activated and regulated by both receptors and has an important role in class-switching to pathological IgG2a in mice. Using primary mouse B cells, we demonstrate that T-bet expression is synergistically elevated by the crosstalk between the BCR and TLR9. To test the effect of this synergy on IgG2a-switching, the levels of switched B cells were checked by functional tests. We found that BCR co-stimulation had no additional effect on TLR9-induced IgG2a expression however the expression of Rad51 was synergistically increased. To check the biological significance of the synergy we compared T-bet expression in B cells from healthy and CIA (collagen-induced arthritis) mice but no differences were found. Taken together, we demonstrate here ...

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WASHINGTON - Some of the worlds largest drugmakers will face an uphill battle next week in their bid to revive a class of experimental arthritis drugs that have been sidelined by safety concerns for nearly two years.. The Food and Drug Administration says there is a clear association between the nerve-blocking medications and incidences of joint failure that led the agency to halt studies of the drugs in 2010. However, the agency also notes that those side effects were less common when the drugs were used at lower doses, potentially leaving the door open for future use. The agency released its safety analysis ahead of a public meeting next week where outside experts will discuss the drugs safety.. On Monday, Pfizer Inc., Johnson & Johnson and Regeneron Pharmaceuticals will make their case to continue studies of the drugs, with safety precautions to protect patients.. The request to restart testing is unusual, since drugmakers often abandon research on experimental drugs that appear to have ...

New data raising safety concerns for Pfizer Incs experimental arthritis drug sent its shares down 3 percent, while lifting shares of rival drugmaker Abbott Laboratories, analysts said.