• Title/Summary/Keyword: Autoimmune arthritis

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Can herbal drug(s) meet the challenges of genomewide screen results on rheumatoid arthritis

  • Paul, Bholanath
    • Advances in Traditional Medicine
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    • v.5 no.4
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    • pp.251-261
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    • 2005
  • Rheumatoid arthritis (RA) is an autoimmune/inflammatory disorder with a complex genetic component. RA is characterized by chronic inflammation of the synovial membrane in the joint, which leads to the progressive destruction of articular cartilage, ligament and bone. Several cytokines such as tumor necrosis $factor-{\alpha}\;TNF-{\alpha}\;and\;interleukin-1{\beta}\;(IL-1{\beta})$ and interleukin-6 (IL-6) have been implicated in the pathological mechanisms of synovial tissue proliferation, joint destruction and programmed cell death in rheumatoid joint. Genome wide screening of subjects suffering from autoimmune diseases especially arthritis revealed linkage to inflammatory molecules like $TNF-{\alpha},\;IL-1{\beta}$ and IL-6, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), nuclear factor-kappaB $(NF-{\kappa}B)$ and human leucocyte antigen/major histocompatibility complex (HLA/MHC) locus. The status of the pharmacological mechanism of herbal drugs in the light of genome wide screening results has been discussed to reinforce the therapeutic potential and the pharmacological basis of the herbal drugs.

Effects of Far Infrared on Nitric Oxide level at a rat model of Autoimmune Arthritis Induced (원적외선이 자가면역성 관절염 흰쥐모델의 산화질소정량에 미치는 영향)

  • Kim Jae Yoon;Park Kyu Hyun;Park Young Han;Kim Jin-Sang;Park Rae Joon
    • The Journal of Korean Physical Therapy
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    • v.14 no.2
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    • pp.65-73
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    • 2002
  • OBJECTIVE: This study was Far infrared(FIR) irradiating to a rat collagen-induced autoimmune arthritis and observed nitric oxide level of spine. METHODS: Type II collagen(CII) in adjuvant was injected into rats on day 0. The results showed that rats injected with CII plus adjuvant had signs of autoimmune arthritis on day 14. Thereafter, Far infrared(FIR) irradiation was begun on day 15. The rats were irradiated FIR twice per day for 20 min each time. RESULTS: Seven days later(Day 22), the level of NO at FIR irradiated group(FRG; Arth+FIR) was decreased more than FIR-non irradiated group(FNRG; Arth). Twenty-one days later(Day 36), the level of NO at FRG was more closed to the control group's NO level than the FNRG. CONCLUSION: These results indicated that Far infrared irradiating appears to reduce the nitric oxide level at a rat model of autoimmune arthritis induced.

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Deficiency of $Foxp3^+$ Regulatory T Cells Exacerbates Autoimmune Arthritis by Altering the Synovial Proportions of $CD4^+$ T Cells and Dendritic Cells

  • Jang, Eun-Kyeong;Cho, Mi-La;Oh, Hye-Joa;Youn, Jee-Hee
    • IMMUNE NETWORK
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    • v.11 no.5
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    • pp.299-306
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    • 2011
  • Background: $CD4^+Fop3^+$ regulatory T cells (Tregs) are needed to maintain peripheral tolerance, but their role in the development of autoimmune arthritis is still debated. The present study was undertaken to investigate the mechanism by which Tregs influence autoimmune arthritis, using a mouse model entitled K/BxN. Methods: We generated Treg-deficient K/BxNsf mice by congenically crossing K/BxN mice with Foxp3 mutant scurfy mice. The arthritic symptoms of the mice were clinically and histopathologically examined. The proportions and activation of $CD4^+$ T cells and/or dendritic cells were assessed in the spleens, draining lymph nodes and synovial tissue of these mice. Results: K/BxNsf mice exhibited earlier onset and more aggressive progression of arthritis than their K/BxN littermates. In particular, bone destruction associated with the influx of numerous RANKL+ cells into synovia was very prominent. They also contained more memory phenotype $CD4^+$ T cells, more Th1 and Th2 cells, and fewer Th17 cells than their control counterparts. Plasmacytoid dendritic cells expressing high levels of CD86 and CD40 were elevated in the K/BxNsf synovia. Conclusion: We conclude that Tregs oppose the progression of arthritis by inhibiting the development of $RANKL^+$ cells, homeostatically proliferating $CD4^+$ T cells, Th1, Th2 and mature plasmacytoid dendritic cells, and by inhibiting their influx into joints.

Panax ginseng: a candidate herbal medicine for autoimmune disease

  • Lee, Joon-Il;Park, Kyoung Sun;Cho, Ik-Hyun
    • Journal of Ginseng Research
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    • v.43 no.3
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    • pp.342-348
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    • 2019
  • Panax ginseng Meyer (P. ginseng; Korean ginseng) is well known for its medicinal properties. It can alleviate pathological symptoms, promote health, and prevent potential diseases via its anti-inflammatory, antioxidant, homeostatic, and other positive effects on biological metabolism. Although many studies have determined effects of P. ginseng on various diseases, such as cardiovascular, neurological, and immunological diseases, little is known about the effect of P. ginseng on autoimmune diseases. Here, we review a few reports about effects of P. ginseng on autoimmune diseases (e.g., multiple sclerosis, Crohn's disease, ulcerative colitis, atopic dermatitis, and rheumatoid arthritis) and suggest the possibility of P. ginseng as a candidate herbal medicine to prevent and treat autoimmune diseases as well as the need to study it.

The Th17 and Autoimmune Arthritis (Th17과 자가면역 관절염)

  • Cho, Mi-La;Heo, Yu-Jung;Park, Jin-Sil;Lee, Seon-Yeong;Sung, Young-Chul;Kim, Ho-Youn
    • IMMUNE NETWORK
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    • v.7 no.1
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    • pp.10-17
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    • 2007
  • Autoimmune arthritis, such as rheumatoid arthritis (RA), is a chronic inflammatory disorder that primarily affects the joints and then results in their progressive destruction. Effector Th cells have been classified as Th1 and Th2 subsets based on their cytokine expression profiles and immune regulatory function. Another subset of T cells termed Th17 was recendy discovered and known to selectively produce IL-17. Also, Th17 was shown to be generated by TGF${\beta}$ and IL-6 and maintained by IL-23. IL-17 is a proinflammatory cytokine that is considered to involve the development of various inflammatory autoimmune diseases such as RA, asthma, lupus, and allograft rejection. IL-17 is present in the sera, synovial fluids and synovial biopsies of most RA patient. IL-17 activates RA synovial fibroblasts to synthesize IL-6, IL-8 and VEGF via PI3K/Akt and NF-${\kappa}B$ dependent pathway. IL-17 increases IL-6 production, collagen destruction and collagen synthesis. In addition, it not only causes bone resorption but also increases osteoclastogenesis and fetal cartilage destruction. Inhibition of the IL-17 production may contribute a novel therapeutic approach along with potent anti-inflammatory effect and with less immunosuppressive effect on host defenses.

Induction of tolerance against the arthritogenic antigen with type-II collagen peptide-linked soluble MHC class II molecules

  • Park, Yoon-Kyung;Jung, Sundo;Park, Se-Ho
    • BMB Reports
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    • v.49 no.6
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    • pp.331-336
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    • 2016
  • In murine collagen-induced arthritis (CIA), self-reactive T cells can recognize peptide antigens derived from type-II collagen (CII). Activation of T cells is an important mediator of autoimmune diseases. Thus, T cells have become a focal point of study to treat autoimmune diseases. In this study, we evaluated the efficacy of recombinant MHC class II molecules in the regulation of antigen-specific T cells by using a self peptide derived from CII (CII260-274; IAGFKGEQGPKGEPG) linked to mouseI-Aq in a murine CIA model. We found that recombinant I-Aq/CII260-274 molecules could be recognized by CII-specific T cells and inhibit the same T cells in vitro. Furthermore, the development of CIA in mice was successfully prevented by in vivo injection of recombinant I-Aq/CII260-274 molecules. Thus, treatment with recombinant soluble MHC class II molecules in complex with an immunodominant self-peptide might offer a potential therapeutic for chronic inflammation in autoimmune disease such as rheumatoid arthritis.

Structure of a Human Insulin Peptide-HLA-DQ8 Complex and Susceptibility to Type 1 Diabetes

  • Lee, Kon-Ho
    • Proceedings of the Korean Biophysical Society Conference
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    • 2002.06b
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    • pp.16-17
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    • 2002
  • The major histocompatibility complex (MHC) is an important susceptibility locus for many human autoimmune diseases. The structural and functional properties of HLA-DR molecules that are associated with susceptibility to several autoimmune diseases, such as rheumatoid arthritis and multiple sclerosis, have been defined.(omitted)

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Role of inflammasomes in inflammatory autoimmune rheumatic diseases

  • Yi, Young-Su
    • The Korean Journal of Physiology and Pharmacology
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    • v.22 no.1
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    • pp.1-15
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    • 2018
  • Inflammasomes are intracellular multiprotein complexes that coordinate anti-pathogenic host defense during inflammatory responses in myeloid cells, especially macrophages. Inflammasome activation leads to activation of caspase-1, resulting in the induction of pyroptosis and the secretion of pro-inflammatory cytokines including interleukin $(IL)-1{\beta}$ and IL-18. Although the inflammatory response is an innate host defense mechanism, chronic inflammation is the main cause of rheumatic diseases, such as rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), ankylosing spondylitis (AS), and $Sj{\ddot{o}}gren^{\prime}s$ syndrome (SS). Since rheumatic diseases are inflammatory/autoimmune disorders, it is reasonable to hypothesize that inflammasomes activated during the inflammatory response play a pivotal role in development and progression of these diseases. Indeed, previous studies have provided important observations that inflammasomes are actively involved in the pathogenesis of inflammatory/autoimmune rheumatic diseases. In this review, we summarize the current knowledge on several types of inflammasomes during macrophage-mediated inflammatory responses and discuss recent research regarding the role of inflammasomes in the pathogenesis of inflammatory/autoimmune rheumatic diseases. This avenue of research could provide new insights for the development of promising therapeutics to treat inflammatory/autoimmune rheumatic diseases.

Visceral Leishmaniasis Mimicking Autoimmune Hepatitis, Primary Biliary Cirrhosis, and Systemic Lupus Erythematosus Overlap

  • Tunccan, Ozlem Guzel;Tufan, Abdurrahman;Telli, Gulcin;Akyurek, Nalan;Pamukcuoglu, Merve;Yilmaz, Guldal;Hizel, Kenan
    • Parasites, Hosts and Diseases
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    • v.50 no.2
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    • pp.133-136
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    • 2012
  • Visceral leishmaniasis (VL) is a life-threatening infection caused by Leishmania species. In addition to typical clinical findings as fever, hepatosplenomegaly, and cachexia, VL is associated with autoimmune phenomena. To date, VL mimicking or exacerbating various autoimmune diseases have been described, including systemic lupus erythematosus (SLE), rheumatoid arthritis, and autoimmune hepatitis (AIH). Herein, we presented a patient with VL who had overlapping clinical features with SLE, AIH, as well as antimitochondrial antibody (AMA-M2) positive primary biliary cirrhosis.

Effects of Opuntia ficus-indica extract on the activation of immune cells with special reference to autoimmune disease models (손바닥선인장 추출물이 면역계세포의 활성화에 미치는 영향)

  • Shin, Tae-Kyun;Lee, Sun-Joo;Kim, Sae-Je
    • Korean Journal of Veterinary Pathology
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    • v.2 no.1
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    • pp.31-36
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    • 1998
  • The Opuntia ficus-indica extract(OFE) has been claimed to have several therapeutic properties including anti-inflammation and anti-rheumatoid arthritis in oriental medicine but little is known about their effect on macrophages. This study demonstrated that OFE could stimulate TNF-alpha production in cultured macrophages. which is one of important mediators in autoimmune diseases including experimental autoimmune encephalomyelitis(EAE). In vivo study showed that oral administration of OFE exacerbate the onset of clinical paralysis. This finding suggests that OFE stimulates cytokine production and exacerbates autoimmune inflammatory diseases including EAE.

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