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
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 ...
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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 ...
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,
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.
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
BioAssay record AID 184149 submitted by ChEMBL: Inhibition of streptococcal cell wall-washed arthritis model in rats at 30.0 mg/kg peroral dose.
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In this issue, we offer a Q&A between the most recent Past Chair of the Joint Section, Mike Groff, and John Ratliff. We will try to continue to interview each o
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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 ...
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,
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 ...
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 ...
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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.
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)...
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...