• Journal of Korean Traditional Oncology
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• v.10 no.1
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• pp.99-106
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• 2005

Objective: This study was done to treat autoimmune chronic active heaptitis Jaundice patient. Method: I analyzed the medical records of a case of autoimmune chronic active hepatitis Jaundice who had been treated with korean traditional medicines from 1 December 2003 through 6 July 2004. Result: Following the korean traditional medicine method, during taking medicine the hematological markers (aspartate transferase(AST), alanine aminotranferase(ALT), Total bilirubin(T.bili)) were effectively controled.

• Annals of Clinical Neurophysiology
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• v.8 no.1
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• pp.6-15
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• 2006

Intravenous immunoglobulin (IVIg) is the treatment of choice for many autoimmune neuropathic disorders such as Guillain-Barre syndrome (GBS), chronic inflammatory Demyelinating neuropathy (CIDP), and multifocal motor neuropathy (MMN). IVIg is preferred because the adverse reactions are milder and fewer than the other immune-modulating methods such as steroid, other immunosuppressant such as azathioprine, and plasmapheresis. IVIg also has been used in other autoimmune neuromuscular disorders (inflammatory myopathy, myasthenia gravis, and Lambert-Eaton myasthenic syndrome) and has been known as safe and efficient agent in these disorders. Since IVIg would get more indications and be used more commonly, clinicians need to know the detailed mechanism of action, side effects, and practical points of IVIg.

• Annals of Clinical Neurophysiology
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• v.14 no.2
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• pp.76-79
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• 2012

Statin is commonly used for lowering cholesterols and can be myotoxic to cause drug-induced necrotizing myopathy. Statin-induced myopathy ranges from asymptomatic hyperCKemia to lethal rhabdomyolysis but is usually reversed by withdrawal of causative drugs. The patient in this study presented with statin-induced necrotizing myopathy, which was finally improved with immunosuppressive therapy, but not just with drug withdrawal. Since statin can induce myopathy through autoimmune processes, we should consider using immunomodulating agents in cases with statin-induced myopathy, which is refractory to drug withdrawal.

• Journal of Oral Medicine and Pain
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• v.46 no.2
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• pp.63-68
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• 2021

Mucous membrane pemphigoid (MMP) is a heterogeneous group of chronic, autoimmune subepithelial blistering diseases, predominantly involving oral mucosal membrane. Because of its pathophysiology of autoimmune reaction, MMP-related gingivitis would not respond to conventional periodontal treatments. We present a case of a 65-year-old female with a chief complaint of chronic generalized buccal gingivitis, unimproved after periodontal treatment for four months. Based on the clinical findings, histological examination, and direct immunofluorescence microscopy, it was diagnosed as MMP. The symptoms were relieved with immunomodulatory therapy using corticosteroids and the supportive management of professional plaque control. MMP can cause pathological involvement throughout the oral and other mucosae of the body, thus leading to functional impairment through repeated inflammatory cascades. Therefore, accurate diagnosis is essential to properly manage local and possible systemic complications of MMP.

• IMMUNE NETWORK
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• v.16 no.4
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• pp.219-232
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• 2016

Production of high affinity antibodies for antigens is a critical component for the immune system to fight off infectious pathogens. However, it could be detrimental to our body when the antigens that B cells recognize are of self-origin. Follicular helper T, or Tfh, cells are required for the generation of germinal center reactions, where high affinity antibody-producing B cells and memory B cells predominantly develop. As such, Tfh cells are considered as targets to prevent B cells from producing high affinity antibodies against self-antigens, when high affinity autoantibodies are responsible for immunopathologies in autoimmune disorders. This review article provides an overview of current understanding of Tfh cells and discusses it in the context of animal models of autoimmune diseases and allograft rejections for generation of novel therapeutic interventions.

• IMMUNE NETWORK
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• v.20 no.6
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• pp.47.1-47.13
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• 2020

Tetracyclines, which have long been used as broad-spectrum antibiotics, also exhibit a variety of nonantibiotic activities including anti-inflammatory and immunomodulatory properties. Tetracyclines bind to the 30S ribosome of the bacteria and inhibit protein synthesis. Unlike antimicrobial activity, the primary molecular target for the nonantibiotic activity of tetracycline remains to be clarified. Nonetheless, the therapeutic efficacies of tetracyclines, particularly minocycline and doxycycline, have been demonstrated in various animal models of autoimmune disorders, such as multiple sclerosis, rheumatoid arthritis, and asthma. In this study, we summarized the anti-inflammatory and immunomodulatory activities of tetracyclines, focusing on the mechanisms underlying these activities. In addition, we highlighted the on-going or completed clinical trials with reported outcomes.

• IMMUNE NETWORK
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• v.19 no.1
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• pp.4.1-4.16
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• 2019

Long noncoding RNAs (lncRNAs) are non-protein coding RNAs of more than 200 nucleotides in length. Despite the term "noncoding", lncRNAs have been reported to be involved in gene expression. Accumulating evidence suggests that lncRNAs play crucial roles in the regulation of immune system and the development of autoimmunity. lncRNAs are expressed in various immune cells including T lymphocytes, B lymphocytes, macrophages, neutrophils, dendritic cells, and NK cells, and are also involved in the differentiation and activation of these immune cells. Here, we review recent studies on the role of lncRNAs in immune regulation and the differential expression of lncRNAs in various autoimmune diseases.

• Korean Journal of Psychosomatic Medicine
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• v.24 no.2
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• pp.227-235
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• 2016

Objectives : The aims of this study were to know the frequency of cognitive dysfunction among patients with autoimmune thyroid disorders, and to reveal influencing factors on it, especially to clarify association with autoimmune thyroid antibodies. Methods : From sixty-five female patients with autoimmune thyroid disorders, demographic data were obtained by structured interview. Their cognitive funtions were measured using the MMSE-K and the MoCA-K tests. Depression was evaluated by the K-HDRS. Results : 1) Among patients with autoimmune thyroid disorders, 7.69% of them were below 24 on the MMSE-K, while 10.77% were below 22 on the MoCA-K. The frequency of cognitive deficit was not significantly different according to having positivity to antimicrosomal antibodies or not. 2) The antimicrosomal antibody-positive patients had significantly higher antithyroglobulin antibody titers, antimicrosomal antibody titers, and TSH concentration, while had significantly lower free T4 levels(p<0.05, respectively). 3) The total scores of the MMSE-K and the MoCA-K had significant correlation with age, marital status, antithyroglobulin antibody titers and K-HDRS(p<0.05, respectively). 4) The regression analysis revealed that variables such as age, education, autoimmune thyroid antibodies, thyroid function and depression did not influence on cognitive function of patients with autoimmune thyroid disorders. Conclusions : Our results could not support that cognitive function of patients with autoimmune thyroid disorders had correlation with autoimmune thyroid antibodies.

• Archives of Pharmacal Research
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• v.22 no.5
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• pp.437-447
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• 1999

Type I diabetes, also known as insulin-dependent diabetes mellitus (IDDM) results from the destruction of insulin-producing pancreatic $\beta$ cells by a progressive $\beta$ cell-specific autoimmune process. The pathogenesis of autoimmune IDDM has been extensively studied for the past two decades using animal models such as the non-obese diabetic (NOD) mouse and the Bio-Breeding (BB) rat. However, the initial events that trigger the immune responses leading to the selective destruction of the $\beta$ cells are poorly understood. It is thought that $\beta$ cell auto-antigens are involved in the triggering of $\beta$ cell-specific autoimmunity. Among a dozen putative $\beta$ cell autoantigens, glutamic acid decarboxylase (GAD) has bee proposed as perhaps the strongest candidate in both humans and the NOD mouse. In the NOD mouse, GAD, as compared with other $\beta$ cell autoantigens, provokes the earliest T cell proliferative response. The suppression of GAD expression in the $\beta$ cells results in the prevention of autoimmune diabetes in NOD mice. In addition, the major populations of cells infiltrating the iselts during the early stage of insulitis in BB rats and NOD mice are macrophages and dendritic cells. The inactivation of macrophages in NOD mice results in the prevention of T cell mediated autoimmune diabetes. Macrophages are primary contributors to the creation of the immune environment conducive to the development and activation of $\beta$cell-specific Th1-type CD4+ T cells and CD8+ cytotoxic T cells that cause autoimmune diabetes in NOD mice. CD4+ and CD8+ T cells are both believed to be important for the destruction of $\beta$ cells. These cells, as final effectors, can kill the insulin-producing $\beta$ cells by the induction of apoptosis. In addition, CD8+ cytotoxic T cells release granzyme and cytolysin (perforin), which are also toxic to $\beta$ cells. In this way, macrophages, CD4+ T cells and CD8+ T cells act synergistically to kill the $\beta$ cells in conjunction with $\beta$ cell autoantigens and MHC class I and II antigens, resulting in the onset of autoimmune type I diabetes.

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.82-83
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• 2003

In the past it was thought that autoimmunity is mediated by antibodies and immune complexes. It has now become clear that many diseases, especially tissue specific, are T cell mediated or at least T cell dependent. The pathogenesis of cell-mediated autoimmune diseases, such as multiple sclerosis, uveitis, diabetes, arthritis, and others, is thought to be in a large measure driven by interferon-gamma-producing antigen-specific T cells polarized toward the Th1 phenotype. (omitted)