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- 1. 関節リウマチのT細胞標的療法 t cell targeted therapies for rheumatoid arthritis
- 2. 再発性多発性軟骨炎の病因および発症機序 etiology and pathogenesis of relapsing polychondritis
- 3. 関節リウマチの病因 pathogenesis of rheumatoid arthritis
- 4. リウマチ性疾患におけるサイトカインネットワーク：治療の意味 cytokine networks in rheumatic diseases implications for therapy
- 5. リウマチ性疾患におけるサイトカインの役割 role of cytokines in rheumatic diseases
- Cytokine networking of innate immunity cells: a potential target of therapy.
- Striz I, Brabcova E1, Kolesar L1, Sekerkova A1.Author information 1*Department of Clinical and Transplant Immunology, Institute for Clinical and Experimental Medicine, Videnska 1958/9 Prague, Czech Republic.AbstractInnate immune cells, particularly macrophages and epithelial cells, play a key role in multiple layers of immune responses. Alarmins and pro-inflammatory cytokines from the IL (interleukin)-1 and TNF (tumour necrosis factor) families initiate the cascade of events by inducing chemokine release from bystander cells and by the up-regulation of adhesion molecules required for transendothelial trafficking of immune cells. Furthermore, innate cytokines produced by dendritic cells, macrophages, epithelial cells and innate lymphoid cells seem to play a critical role in polarization of helper T-cell cytokine profiles into specific subsets of Th1/Th2/Th17 effector cells or regulatory T-cells. Lastly, the innate immune system down-regulates effector mechanisms and restores homoeostasis in injured tissue via cytokines from the IL-10 and TGF (transforming growth factor) families mainly released from macrophages, preferentially the M2 subset, which have a capacity to induce regulatory T-cells, inhibit the production of pro-inflammatory cytokines and induce healing of the tissue by regulating extracellular matrix protein deposition and angiogenesis. Cytokines produced by innate immune cells represent an attractive target for therapeutic intervention, and multiple molecules are currently being tested clinically in patients with inflammatory bowel disease, rheumatoid arthritis, systemic diseases, autoinflammatory syndromes, fibrosing processes or malignancies. In addition to the already widely used blockers of TNFα and the tested inhibitors of IL-1 and IL-6, multiple therapeutic molecules are currently in clinical trials targeting TNF-related molecules [APRIL (a proliferation-inducing ligand) and BAFF (B-cell-activating factor belonging to the TNF family)], chemokine receptors, IL-17, TGFβ and other cytokines.
- Clinical science (London, England : 1979).Clin Sci (Lond).2014 May 1;126(9):593-612. doi: 10.1042/CS20130497.
- Innate immune cells, particularly macrophages and epithelial cells, play a key role in multiple layers of immune responses. Alarmins and pro-inflammatory cytokines from the IL (interleukin)-1 and TNF (tumour necrosis factor) families initiate the cascade of events by inducing chemokine release from
- PMID 24450743
- Localizer sequences of magnetic resonance imaging accurately identify osteoporotic vertebral fractures.
- Bazzocchi A1, Garzillo G2, Fuzzi F2, Diano D2, Albisinni U3, Salizzoni E2, Battista G2, Guglielmi G4.Author information 1Department of Specialized, Diagnostic, and Experimental Medicine, University of Bologna, Sant'Orsola-Malpighi Hospital, Via G. Massarenti 9, 40138 Bologna, Italy; Diagnostic and Interventional Radiology, "Rizzoli" Orthopaedic Institute, Via G. C. Pupilli 1, 40136 Bologna, Italy.2Department of Specialized, Diagnostic, and Experimental Medicine, University of Bologna, Sant'Orsola-Malpighi Hospital, Via G. Massarenti 9, 40138 Bologna, Italy.3Diagnostic and Interventional Radiology, "Rizzoli" Orthopaedic Institute, Via G. C. Pupilli 1, 40136 Bologna, Italy.4Department of Radiology, University of Foggia, Viale Luigi Pinto 1, 71100 Foggia, Italy; Department of Radiology, Scientific Institute "Casa Sollievo della Sofferenza" Hospital, Viale Cappuccini 1, 71013 San Giovanni Rotondo, Foggia, Italy. Electronic address: firstname.lastname@example.org.AbstractThe aim of the present study was to evaluate the performance of sagittal MR localizer (MR-loc), in terms of diagnostic accuracy and intra- and inter-observer agreement in the detection of vertebral fractures (VFs). Three-hundred MR examinations of the thoracic and/or lumbar spine were randomly collected. A semi-quantitative approach was used and morphometric analysis was performed when a VF was suspected. MR-loc images were evaluated blindly by three radiologists in two different sessions. A full diagnostic sagittal T1-weighted fast spin echo MR sequence was used as standard of reference (RS). Degenerative arthritis was also scored on RS. Only vertebral bodies which were assessable by both MR-loc and RS were considered for the analysis. Area under the receiver operating characteristic curve (AUROC), Cohen kappa statistic, and linear-by-linear association were used for statistical analysis. Kappa values were compared by means of the z distribution. A total of 2186 vertebrae were analysed in 300 MRI exams (147 males, 153 females, 59.4±16.4y.o.). Sixty-seven out of 2136 (3.1%) VFs were identified in 23/300 (7.7%) patients submitted to MRI. In the detection of VFs, sensitivity and specificity of MR-loc were both 100% (accuracy AUROC=1.000). Inter-observer agreement was excellent (k=0.938±0.013), while intra-observer agreement was perfect (k=1.000). The diagnostic performance was independent from degenerative arthritis, vertebral level, type and grade of VFs. MR-loc is a simple but accurate tool in the detection of VFs. It should be introduced for systematic evaluation in the detection of VFs in MR examinations performed in daily clinical practice.
- Bone.Bone.2014 Apr;61:158-63. doi: 10.1016/j.bone.2014.01.013. Epub 2014 Jan 25.
- The aim of the present study was to evaluate the performance of sagittal MR localizer (MR-loc), in terms of diagnostic accuracy and intra- and inter-observer agreement in the detection of vertebral fractures (VFs). Three-hundred MR examinations of the thoracic and/or lumbar spine were randomly colle
- PMID 24473374
- Siglec-G Deficiency Leads to More Severe Collagen-Induced Arthritis and Earlier Onset of Lupus-like Symptoms in MRL/lpr Mice.
- Bökers S1, Urbat A, Daniel C, Amann K, Smith KG, Espéli M, Nitschke L.Author information 1Division of Genetics, Department of Biology, University of Erlangen-Nürnberg, 91058 Erlangen, Germany;AbstractSiglec-G is a member of the sialic acid-binding Ig-like lectin (Siglec) family expressed on all B cells. Siglec-G-deficient mice show a large expansion of the B1 cell compartment, demonstrating the crucial role of Siglec-G as an inhibitory receptor on this cellular subset. Although Siglec-G-deficient mice did not develop spontaneous autoimmunity, mice double-deficient for Siglec-G and the related Siglec protein CD22 did show autoimmunity at an older age. In this study, we addressed the question of whether loss of Siglec G on its own affects disease severity in animal models of rheumatoid arthritis and systemic lupus erythematosus. Siglec-G-deficient mice showed moderately increased clinical severity and higher inflammation of the knee joints following collagen-induced arthritis, when compared with control mice. The Siglec-G-deficient mouse was also backcrossed to the autoimmune prone MLR/lpr background. Although both Siglec-G-deficient and control MRL/lpr mice developed a lupus-like disease, Siglec-G-deficient MRL/lpr mice showed an earlier occurrence of autoantibodies; a higher lymphoproliferation of B and T cells; and an earlier onset of disease, as shown by proteinuria and glomerular damage in the kidney. Moreover, Siglec-G-deficient female mice showed a significantly reduced survival compared with female control MRL/lpr mice. Thus, the loss of the inhibitory receptor Siglec-G led to a moderate exacerbation of disease severity and early onset in both collagen-induced arthritis and spontaneous lupus nephritis in MRL/lpr mice.
- Journal of immunology (Baltimore, Md. : 1950).J Immunol.2014 Mar 5. [Epub ahead of print]
- Siglec-G is a member of the sialic acid-binding Ig-like lectin (Siglec) family expressed on all B cells. Siglec-G-deficient mice show a large expansion of the B1 cell compartment, demonstrating the crucial role of Siglec-G as an inhibitory receptor on this cellular subset. Although Siglec-G-deficien
- PMID 24600033
- Lipopolysaccharide accelerates collagen-induced arthritis in association with rapid and continuous production of inflammatory mediators and anti-type Ⅱ collagen antibody
- Tanaka Shinji,Toki Tadashi,Akimoto Toshihiko [他]
- Microbiology and immunology 57(6), 445-454, 2013-06
- NAID 40019700929
- The long-term immunosuppressive effects of disulfide-linked HLA-G dimer in mice with collagen-induced arthritis
- Kuroki Kimiko,Hirose Kaoru,Okabe Yuki,Fukunaga Yuko,Takahashi Ami,Shiroishi Mitsunori,Kajikawa Mizuho,Tabata Shigekazu,Nakamura Seiko,Takai Toshiyuki,Koyanagi Satoru,Ohdo Shigehiro,Maenaka Katsumi
- HUMAN IMMUNOLOGY 74(4), 433-438, 2013-04
- … In this report, we studied the in vivo immunosuppressive effect of the HLA-G dimer, using the collagen-induced arthritis model mouse. … The HLA-G dimer is expected to be quite useful as an anti-rheumatoid arthritis agent, in small amounts with minimal side effects. …
- NAID 120005297913
- Etanercept promotes bone formation via suppression of dickkopf-1 expression in rats with collagen-induced arthritis
- Tanida Atsushi,Kishimoto Yuji,Okano Toru,Hagino Hiroshi
- Yonago Acta medica 56(1), 13-19, 2013-03
- NAID 120005263096
- ... mouse model is the most commonly studied autoimmune model of rheumatoid arthritis. Autoimmune arthritis is induced in this model by immunization with an emulsion of complete Freund's adjuvant and type II collagen (CII ...
- 1. Methods Mol Biol. 2010;602:181-92. doi: 10.1007/978-1-60761-058-8_11. Collagen-induced arthritis in mice. Bevaart L(1), Vervoordeldonk MJ, Tak PP. Author information: (1)Division of Clinical Immunology ...
|リンク元||「CIA」「コラーゲン関節炎」「adjuvant arthritis」「adjuvant-induced arthritis」「collagen arthritis」|
- hypercalcaemia induced pancreatitis 高カルシウム血症による膵炎