• Journal of Pharmacopuncture
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• v.23 no.4
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• pp.187-193
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• 2020

Objectives: It was aimed to investigate the basic action mechanism of the autoimmune diseases and common features of all diseases. Autoimmune disease are classified organ specific and systemic. Methods: These diseases are seen systemic and disease start locations, origins seem differently. This makes learning and understanding difficult. Autoimmune diseases investigated for easier understanding. It was noticed that, autoimmune diseases' starting places are specific and same all of them. This remarkable point is very important for acupuncture also. So; whole literatüre was researched and important point was found. Results: Whole autoimmune diseases are attack to mesodermal layers and mesodermal origin organs of the body's. The common property of all these disease are same; Diseases start from the mesoderm and mesodermal layer even though their organ origins' belongs to different germ layer. From this point of view, we were able to classify autoimmune diseases simply and it was planned how can we effect body in this context with acupuncture. Conclusion: And, when immunity comes into question, induction of adaptive immunity is depend on antigen presentation to T cells and this situation take place in the lymph node (LN) and also in the skin.When we sank the acupuncture needle into skin, signals create and start mesodermal contacts, during this time mesenchymal origin' autoimmune cells are regulated with this signals.

• Korean Journal of Biological Psychiatry
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• v.15 no.3
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• pp.152-174
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• 2008

There have been vast amount studies regarding immunologic dysregulation in schizophrenia. The mechanism of immune pathogenesis in schizophrenia still is unclear, even though various immune dysfunction have been reported. We endeavored to report on two major hypothesis on immunologic dysregulation in schizophrenia, the infection hypothesis and autoimmune hypothesis. We went on to focus on the autoimmune hypothesis, which has received the most attention over the years. We explored the accumulated data and the rational behind the autoimmune hypothesis and the implications of the autoimmune hypothesis for future research in the pathogenesis of schizophrenia.

• 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.

• BMB Reports
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• v.55 no.2
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• pp.57-64
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• 2022

Autoimmune disease is known to be caused by unregulated self-antigen-specific T cells, causing tissue damage. Although antigen specificity is an important mechanism of the adaptive immune system, antigen non-related T cells have been found in the inflamed tissues in various conditions. Bystander T cell activation refers to the activation of T cells without antigen recognition. During an immune response to a pathogen, bystander activation of self-reactive T cells via inflammatory mediators such as cytokines can trigger autoimmune diseases. Other antigen-specific T cells can also be bystander-activated to induce innate immune response resulting in autoimmune disease pathogenesis along with self-antigen-specific T cells. In this review, we summarize previous studies investigating bystander activation of various T cell types (NKT, γδ T cells, MAIT cells, conventional CD4⁺, and CD8⁺ T cells) and discuss the role of innate-like T cell response in autoimmune diseases. In addition, we also review previous findings of bystander T cell function in infection and cancer. A better understanding of bystander-activated T cells versus antigen-stimulated T cells provides a novel insight to control autoimmune disease pathogenesis.

• Journal of Acupuncture Research
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• v.18 no.6
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• pp.232-239
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• 2001

Objective & Method : To identify current state of bee venom therapy(BVT) research as a treatment of autoimmune diseases, we reviewed the PubMed electronic database. 9 articles with clinical implications were discussed. Results : BVT is reported as effective in the treatment of such autoimmune related diseases as rheumatoid arthritis and insulin dependent diabetes mellitus in animal experiment, The lack of evidence on BVT as a treatment of multiple sclerosis deters us from reaching any determination. There also lacks firm evidences of immune response regulative or anti inflammatory mechanism of BVT. No clinicla trial was found. Conculsion : This review raises the urgent need of study to provide scientific and clinical evidences.

• 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.

• 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.

• Advances in Traditional Medicine
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• v.8 no.1
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• pp.1-16
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• 2008

Immunity is responsible for the defense mechanism of the body but in case of autoimmune diseases, its role gets diverted. Like so many other diseases, asthma is also considered as one of the most common autoimmune diseases to be occurring in community. Asthma is defined as a chronic inflammatory airway disease that is characterized by airway hyper reactivity and mucus hypersecretion that result in intermittent airway obstruction. The incidence of allergic asthma has almost doubled in the past two decades. Although, precise causative mechanism of asthma is unknown, but several mechanisms have been proposed that is immunological, pharmacological and genetic mechanisms, and airway and neurogenic inflammation. The inflammatory process observed in the asthmatic patients is the final result of a complex network of interactions between various immunological cell lineages, its mediators and secreted substances. Thus, among the mechanisms proposed, the immunological one plays a key role. Through this article, we have tried to provide some insight into immunological mechanisms in pathogenesis of asthma.

• Journal of Ginseng Research
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• v.42 no.4
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• pp.436-446
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• 2018

Background: The potential therapeutic values of Korean Red Ginseng extract (KRGE) in autoimmune disorders of nervous system have not been fully investigated. Methods: We used an acute experimental autoimmune encephalomyelitis animal model of multiple sclerosis and determined the effects and mechanism of KRGE on spinal myelination. Results: Pretreatment with KRGE (100 mg/kg, orally) for 10 days before immunization with myelin basic protein $(MBP)_{68-82}$ peptide exerted a protective effect against demyelination in the spinal cord, with inhibited recruitment and activation of immune cells including microglia, decreased mRNA expression of detrimental inflammatory mediators (interleukin-6, interferon-${\gamma}$, and cyclooxygenase-2), but increased mRNA expression of protective inflammatory mediators (insulin-like growth factor ${\beta}1$, transforming growth factor ${\beta}$, and vascular endothelial growth factor-1). These results were associated with significant downregulation of p38 mitogen-activated protein kinase and nuclear factor-${\kappa}B$ signaling pathways in microglia/macrophages, T cells, and astrocytes. Conclusion: Our findings suggest that KRGE alleviates spinal demyelination in acute experimental autoimmune encephalomyelitis through inhibiting the activation of the p38 mitogen-activated protein kinase/nuclear factor-${\kappa}B$ signaling pathway. Therefore, KRGE might be used as a new therapeutic for autoimmune disorders such as multiple sclerosis, although further investigation is needed.

• IMMUNE NETWORK
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• v.23 no.2
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• pp.12.1-12.17
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• 2023

Ssu72, a dual-specificity protein phosphatase, not only participates in transcription biogenesis, but also affects pathophysiological functions in a tissue-specific manner. Recently, it has been shown that Ssu72 is required for T cell differentiation and function by controlling multiple immune receptor-mediated signals, including TCR and several cytokine receptor signaling pathways. Ssu72 deficiency in T cells is associated with impaired fine-tuning of receptor-mediated signaling and a defect in CD4⁺ T cell homeostasis, resulting in immune-mediated diseases. However, the mechanism by which Ssu72 in T cells integrates the pathophysiology of multiple immune-mediated diseases is still poorly elucidated. In this review, we will focus on the immunoregulatory mechanism of Ssu72 phosphatase in CD4⁺ T cell differentiation, activation, and phenotypic function. We will also discuss the current understanding of the correlation between Ssu72 in T cells and pathological functions which suggests that Ssu72 might be a therapeutic target in autoimmune disorders and other diseases.