• 제목/요약/키워드: autoimmune

검색결과 709건 처리시간 0.021초

자가 면역 갑상선 질환에 대한 최대 표준섭취계수와 갑상선 자가 항체의 임상적 상관관계: 하시모토 갑상선염과 그레이브스병 중심으로 (Clinical Correlation between the Autoimmune Thyroid Disease for the Thyroid Autoimmune Antibodies and the Maximum Standardized Uptake Value: Base on the Hashimoto's Thyroiditis and the Graves' Disease)

  • 우민선;백철인;유주은;송종우;임인철;손주철;조수동;이재승
    • 한국방사선학회논문지
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    • 제8권5호
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    • pp.241-248
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    • 2014
  • 본 연구는 미만성 $^{18}F-FDG$ 갑상선 섭취를 보이는 PET/CT 영상에서 최대 표준섭취계수($SUV_{max}$)와 갑상선 자가 항체(anti-TPO Ab, anti-TG Ab, TSH)들 사이의 임상적 상관관계를 하시모토 갑상선염과 그레이브스병 중심으로 분석하였다. 이를 위하여 2010년 5월부터 2013년 4월까지 건강검진에서 PET/CT 검사를 시행한 환자 1,097명을 대상으로 미만성 FDG 갑상선 섭취 여부를 분석하여 갑상선 기능 검사와 초음파 검사를 추가적으로 시행하였다. 결과적으로 미만성 $^{18}F-FDG$ 갑상선 섭취를 보이는 자가 면역 갑상선 질환 환자는 39명(3.6%)이 발견되었으며 하시모토 갑상선염은 43.6%, 그레이브스병은 23.1% 이었다. 하시모토 갑상선염은 anti-TPO Ab와 anti-TG 수준이 높은 역가의 양성 반응을 보였으며 $SUV_{max}$와 anti-TPO Ab간 상관계수가 통계적으로 유의하였다(r>0.4, p<0.05). 또한 그레이브스병은 대부분의 갑상선 자가 항체의 수준이 높은 역가의 양성 반응을 보였으며 $SUV_{max}$와 TSH간 상관계수가 통계적으로 유의하였다(r>0.5, p<0.01). 따라서 미만성 18F-FDG 갑상선 섭취 증가에 따른 $SUV_{max}$ 수준이 높을수록 하시모토 갑상선염은 anti-TPO Ab 수준이, 그레이브스병은 TSH 수준이 비례적으로 증가됨을 알 수 있었고 이러한 상관관계는 자가 면역 갑상선 질환에 대한 부대 징후를 판단할 수 있는 가장 영향력 있는 척도로서 임상적 적용이 가능할 것으로 판단하였다.

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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    • 제49권6호
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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.

MicroRNAs in Human Diseases: From Autoimmune Diseases to Skin, Psychiatric and Neurodegenerative Diseases

  • Ha, Tai-You
    • IMMUNE NETWORK
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    • 제11권5호
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    • pp.227-244
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    • 2011
  • MicroRNAs (miRNAs) are small noncoding RNA molecules that negatively regulate gene expression via degradation or translational repression of their target messenger RNAs (mRNAs). Recent studies have clearly demonstrated that miRNAs play critical roles in several biologic processes, including cell cycle, differentiation, cell development, cell growth, and apoptosis and that miRNAs are highly expressed in regulatory T (Treg) cells and a wide range of miRNAs are involved in the regulation of immunity and in the prevention of autoimmunity. It has been increasingly reported that miRNAs are associated with various human diseases like autoimmune disease, skin disease, neurological disease and psychiatric disease. Recently, the identification of miRNAs in skin has added a new dimension in the regulatory network and attracted significant interest in this novel layer of gene regulation. Although miRNA research in the field of dermatology is still relatively new, miRNAs have been the subject of much dermatological interest in skin morphogenesis and in regulating angiogenesis. In addition, miRNAs are moving rapidly center stage as key regulators of neuronal development and function in addition to important contributions to neurodegenerative disorder. Moreover, there is now compelling evidence that dysregulation of miRNA networks is implicated in the development and onset of human neruodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, Tourette's syndrome, Down syndrome, depression and schizophrenia. In this review, I briefly summarize the current studies about the roles of miRNAs in various autoimmune diseases, skin diseases, psychoneurological disorders and mental stress.

A New Approach to Managing Oral Manifestations of Sjogren's Syndrome and Skin Manifestations of Lupus

  • Hsu, Stephen;Dickinson, Douglas
    • BMB Reports
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    • 제39권3호
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    • pp.229-239
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    • 2006
  • Sj$\"{o}$gren's syndrome (SS) is an autoimmune disorder that affects the salivary glands, leading to xerostomia, and the lacrimal glands, resulting in xerophthalmia. Secondary SS is associated with other autoimmune disorders such as systemic rheumatic diseases and systemic lupus erythematosis (SLE), which can affect multiple organs, including the epidermis. Recent studies have demonstrated that green tea polyphenols (GTPs) possess both anti-inflammatory and anti-apoptotic properties in normal human cells. Epidemiological evidence has indicated that, in comparison to the United States, the incidence of SS, clinical xerostomia and lupus is considerably lower in China and Japan, the two leading green tea-consuming countries. Thus, GTPs might be responsible, in part, for geographical differences in the incidence of xerostomia by reducing the initiation or severity of SS and lupus. Consistent with this, molecular, cellular and animal studies indicate that GTPs could provide protective effects against autoimmune reactions in salivary glands and skin. Therefore, salivary tissues and epidermal keratinocytes could be primary targets for novel therapies using GTPs. This review article evaluates the currently available research data on GTPs, focusing on their potential application in the treatment of the oral manifestations of SS and skin manifestations of SLE.

Expression of Cholera Toxin B Subunit and Assembly as Functional Oligomers in Silkworm

  • Gong, Zhao-Hui;Jin, Hui-Qing;Jin, Yong-Feng;Zhang, Yao-Zhou
    • BMB Reports
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    • 제38권6호
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    • pp.717-724
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    • 2005
  • The nontoxic B subunit of cholera toxin (CTB) can significantly increase the ability of proteins to induce immunological tolerance after oral administration, when it was conjugated to various proteins. Recombinant CTB offers great potential for treatment of autoimmune disease. Here we firstly investigated the feasibility of silkworm baculovirus expression vector system for the cost-effective production of CTB under the control of a strong polyhedrin promoter. Higher expression was achieved via introducing the partial non-coding and coding sequences (ATAAAT and ATGCCGAAT) of polyhedrin to the 5' end of the native CTB gene, with the maximal accumulation being approximately 54.4 mg/L of hemolymph. The silkworm bioreactor produced this protein vaccine as the glycoslated pentameric form, which retained the GM1-ganglioside binding affinity and the native antigenicity of CTB. Further studies revealed that mixing with silkworm-derived CTB increases the tolerogenic potential of insulin. In the nonconjugated form, an insulin : CTB ratio of 100 : 1 was optimal for the prominent reduction in pancreatic islet inflammation. The data presented here demonstrate that the silkworm bioreactor is an ideal production and delivery system for an oral protein vaccine designed to develop immunological tolerance against autoimmune diabetes and CTB functions as an effective mucosal adjuvant for oral tolerance induction.

Successful Treatment of a Korean Infant with Giant Cell Hepatitis with Autoimmune Hemolytic Anemia Using Rituximab

  • Kim, Young Ho;Kim, Ju Whi;Lee, Eun Joo;Kang, Gyeong Hoon;Kang, Hyoung Jin;Moon, Jin Soo;Ko, Jae Sung
    • Pediatric Gastroenterology, Hepatology & Nutrition
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    • 제23권2호
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    • pp.180-187
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    • 2020
  • Giant cell hepatitis with autoimmune hemolytic anemia (AHA) is a rare disease of infancy characterized by the presence of both Coombs-positive hemolytic anemia and progressive liver disease with giant cell transformation of hepatocytes. Here, we report a case involving a seven-month-old male infant who presented with AHA followed by cholestatic hepatitis. The clinical features included jaundice, pallor, and red urine. Physical examination showed generalized icterus and splenomegaly. The laboratory findings suggested warm-type AHA with cholestatic hepatitis. Liver biopsy revealed giant cell transformation of hepatocytes and moderate lobular inflammation. The patient was successfully treated with four doses of rituximab. Early relapse of hemolytic anemia and hepatitis was observed, which prompted the use of an additional salvage dose of rituximab. He is currently in clinical remission.

Lymphocγtic Interstitial Pneumonia 1예 (A Case of Lymphocytic Interstitial Pneumonia)

  • 서요안;김상일;김대한;곽진영;이재철;백희종;정진행
    • Tuberculosis and Respiratory Diseases
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    • 제51권4호
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    • pp.390-394
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    • 2001
  • Lymphocytic interstitial pneumonia(LIP) is characterized by a massive infiltration of the interstitium of the lung by mature lymphocytes, plasma cells and reticuloendothelial cells. LIP may be associated with autoimmune diseases including Sj$\check{o}$grens syndrome, SLE, myasthenia gravis, pernicious anemia, autoimmune hemolytic anemia, and HIV or an EB virus infection. There is a possibility of LIP progressing to a pulmonary or systemic lymphoma. The therapeutic response to corticosteroids and/or immunosuppressive drugs varies. Here we report a case of LIP that was diagnosed by an open lung biopsy and clonality study. The patient was a 36 year-old man without autoimmune disease or HIV infection. He was admitted as a result of severe hypoxemia showing $PaO_2$ of 48.3mmHg. The patient was treated with corticosteroids after the diagnosis and had fully recovered without a sequalae or relapse.

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Type 1 diabetes genetic susceptibility markers and their functional implications

  • Park, Yongsoo
    • Journal of Genetic Medicine
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    • 제11권1호
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    • pp.1-10
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    • 2014
  • Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by selective destruction of pancreatic ${\beta}$-cells resulting in insulin deficiency. The genetic determinants of T1D susceptibility have been linked to several loci, in particular to the human leukocyte antigen (HLA) region, which accounts for 50% of the genetic risk of developing T1D. Multiple genes in the HLA region, which are in strong linkage disequilibrium, are thought to be involved. Another important locus, with a smaller effect on genetic predisposition to T1D, is the insulin gene. The advent of numerous single nucleotide polymorphism markers and genome screening has enabled the identification of dozens of new T1D susceptibility loci. Some of them appear to predispose to T1D independently of the HLA and may be important in families with T1D who lack strong HLA susceptibility. Other loci may interact with each other to cause susceptibility. The autoimmune response against ${\beta}$-cells can also be triggered by environmental factors in the presence of a predisposing genetic background. Deciphering the environmental and genetic factors involved should help to understand the origin of T1D and aid in the design of individualized prevention programs.

자기면역성 뇌척수염에서 interleukin-1β converting enzyme의 발현 (The expression of interleukin-1β converting enzyme in experimental autoimmune encephalomyelitis)

  • 문창종;김승준;이용덕;신태균
    • 대한수의학회지
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    • 제39권3호
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    • pp.538-544
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    • 1999
  • To elucidate the involvement of interleukin-$1{\beta}$ converting enzyme (ICE) in the course of experimental autoimmune encephalomyelitis (EAE), we induced EAE by immunizing rats with an emulsion of rat spinal cord homogenate with complete Freund's adjuvant supplemented with Mycobacterium tuberculosis (H37Ra, 5mg/ml) and then examined the expression of ICE in the spinal cord of rats with EAE. In normal rat spinal cords, ICE is constitutively, but weakly, expressed in ependymal cells, neurons, and some neuroglial cells. In EAE, many inflammatory cells are positive for ICE, and the majority of ICE+ cells were identified as ED1+ macrophages. During this stage of EAE, the number of ICE+ cells in brain cells, including neurons and astrocytes, increased and these cells also had increased ICE immunoreactivity. These findings suggest that the upregulation of ICE in both brain cells and invading hematogenous cells is stimulated by a secretory product from inflammatory cells, and that this enzyme is involved in the pathogenesis of EAE via the production of IL-1 beta.

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Neuroprotective Effects of 6-Shogaol and Its Metabolite, 6-Paradol, in a Mouse Model of Multiple Sclerosis

  • Sapkota, Arjun;Park, Se Jin;Choi, Ji Woong
    • Biomolecules & Therapeutics
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    • 제27권2호
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    • pp.152-159
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    • 2019
  • Multiple sclerosis (MS) is an autoimmune disease characterized by progressive neuronal loss, neuroinflammation, axonal degeneration, and demyelination. Previous studies have reported that 6-shogaol, a major constituent of ginger (Zingiber officinale rhizome), and its biological metabolite, 6-paradol, have anti-inflammatory and anti-oxidative properties in the central nervous system (CNS). In the present study, we investigated whether 6-shogaol and 6-paradol could ameliorate against experimental autoimmune encephalomyelitis (EAE), a mouse model of MS elicited by myelin oligodendrocyte glycoprotein ($MOG_{35-55}$) peptide immunization with injection of pertussis toxin. Once-daily administration of 6-shogaol and 6-paradol (5 mg/kg/day, p.o.) to symptomatic EAE mice significantly alleviated clinical signs of the disease along with remyelination and reduced cell accumulation in the white matter of spinal cord. Administration of 6-shogaol and 6-paradol into EAE mice markedly reduced astrogliosis and microglial activation as key features of immune responses inside the CNS. Furthermore, administration of these two molecules significantly suppressed expression level of tumor necrosis $factor-{\alpha}$, a major proinflammatory cytokine, in EAE spinal cord. Collectively, these results demonstrate therapeutic efficacy of 6-shogaol or 6-paradol for EAE by reducing neuroinflammatory responses, further indicating the therapeutic potential of these two active ingredients of ginger for MS.