• 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.

• 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.

• Journal of Life Science
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• v.13 no.2
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• pp.236-240
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• 2003

Human immune system acts to protect the host from infectious agents (bacteria, viruses, fungi, parasites) and from other noxious insults. However, immune diseases are sometimes caused by the impairment of immune system leading to abnormal immune response. Especially, autoimmune diseases are very diverse and often bring serious damage Although many active investigations to reveal the etiological mechanisms concerning the autoimmune diseases, it still remains unclear. After proposing a HERV (human endogenous retrovirus) as a candidate autoimmune gene in type I diabetes, it is newly attracting our attention for demonstrating that an endogenous human retroviral superantigen can be transactivated by interferon-$\alpha$ (IFN- $\alpha$) or Epstein-Barr virus (EBV) infection. These might provide us with powerful clues to carry out further studies to overcome autoimmune diseases as the presentation of a relatively clear connection between endogenous superantigens and human diseases.

• The Journal of the Korea Contents Association
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• v.17 no.7
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• pp.648-663
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• 2017

To verify the association between GSTM1/GSTT1 gene polymorphisms and susceptibility to autoimmune diseases in Asian population. 18 published reports cited in EMBASE, Google, KISS, MEDLINE and PubMed up to December 2015 were collected for a meta-analysis. The GSTM1/GSTT1 polymorphism for null and present type were analysed separately. The significant association was found between the GST polymorphism and autoimmune diseases in an overall population (GSTM1, OR=1.334, 95% CI=1.137-1.567, p=0.000; GSTT1, OR=1.212, 95% CI=1.012-1.452, p=0.037). Asian population showed the significant association of GSTM1 in the autoimmune diseases, especially vitiligo and atopic dermatitis but non-significant association of GSTT1 in RA and SLE. The GSTM1 null and the GSTT1 present type showed the association with autoimmune diseases in Asian population. The null type frequency of the combination of GSTM1-GSTT1 polymorphism in autoimmune diseases in Asian population was higher than that of the control group. This result indicated that null type of GSTM1-GSTT1 combination can be a risk factor of autoimmune diseases in Asian population.

• 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.

• Molecules and Cells
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• v.42 no.11
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• pp.747-754
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• 2019

The incidence of atherosclerosis is higher among patients with several autoimmune diseases such as psoriasis, rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). It is well documented that innate immune cells including macrophages and dendritic cells sense lipid species such as saturated fatty acids and oxidized low-density lipoprotein and produce pro-inflammatory cytokines and chemokines. However, whether a hyperlipidemic environment also impacts autoimmune T cell responses has been unclear. Among $CD4^+$ T cells, Th17 and follicular helper T (Tfh) cells are known to play pathogenic roles in the development of hyperlipidemia-associated autoimmune diseases. This review gives an overview of the cellular and molecular mechanisms by which dysregulated lipid metabolism impacts the pathogenesis of autoimmune diseases, with specific emphasis on Th17 and Tfh cells.

• IMMUNE NETWORK
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• v.22 no.5
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• pp.37.1-37.16
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• 2022

Autoimmune diseases are caused by a dysfunction of the acquired immune system. In a subset of autoimmune diseases, B cells escaping immune tolerance present autoantigen and produce cytokines and/or autoantibodies, resulting in systemic or organ-specific autoimmunity. Therefore, B cell depletion with monoclonal Abs targeting B cell lineage markers is standard care therapy for several B cell-mediated autoimmune disorders. In the last 5 years, genetically-engineered cellular immunotherapies targeting B cells have shown superior efficacy and long-term remission of B cell malignancies compared to historical clinical outcomes using B cell depletion with monoclonal Ab therapies. This has raised interest in understanding whether similar durable remission could be achieved with use of genetically-engineered cell therapies for autoimmunity. This review will focus on current human clinical trials using engineered cell therapies for B cell-associated autoimmune diseases.

• Annals of Clinical Neurophysiology
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• v.3 no.1
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• pp.21-25
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• 2001

Background & Object : Myasthenia gravis(MG) is an autoimmune disease due to binding of antibody to acetylcholine receptors on the muscle membrane. It is well known that other autoimmune diseases infrequently accompany myasthenia gravis. The aim of this study was to evaluate the clinical significance of associated autoimmune diseases(AAD) and compare prognosis between MG with AAD and MG without AAD. Method : A total of 65 MG patients(24 men and 41 women) were enrolled at this study. From the clinical records of these patients, we investigated the clinical characteristics and prognosis of MG with AAD and compared these data with those of MG without other such diseases. Results : AAD were found in 10 of 65 cases(15%). 9 cases of 10 MG with AAD were generalized MG type. The most common disease was thyroid disorder. The rate of AAD was higher in thymic abnormal patients. There was no significant remission rate difference between MG with AAD and MG without AAD, but the percentage of patients experienced crisis was higher in MG with AAD. Conclusion : The occurrence of AAD may suggest a more generalized autoimmune disturbance that could be associated with a less favorable prognosis.

• IMMUNE NETWORK
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• v.22 no.1
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• pp.9.1-9.23
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• 2022

In the past few decades, biological drugs and small molecule inhibitors targeting inflammatory cytokines, immune cells, and intracellular kinases have become the standard-of-care to treat autoimmune diseases. Inhibition of TNF, IL-6, IL-17, and IL-23 has revolutionized the treatment of autoimmune diseases, such as rheumatoid arthritis, ankylosing spondylitis, and psoriasis. B cell depletion therapy using anti-CD20 mAbs has shown promising results in patients with neuroinflammatory diseases, and inhibition of B cell survival factors is approved for treatment of systemic lupus erythematosus. Targeting co-stimulatory molecules expressed on Ag-presenting cells and T cells is also expected to have therapeutic potential in autoimmune diseases by modulating T cell function. Recently, small molecule kinase inhibitors targeting the JAK family, which is responsible for signal transduction from multiple receptors, have garnered great interest in the field of autoimmune and hematologic diseases. However, there are still unmet medical needs in terms of therapeutic efficacy and safety profiles. Emerging therapies aim to induce immune tolerance without compromising immune function, using advanced molecular engineering techniques.

• IMMUNE NETWORK
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• v.8 no.4
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• pp.107-123
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• 2008

It has now been well documented in a variety of models that T regulatory T cells (Treg cells) play a pivotal role in the maintenance of self-tolerance, T cell homeostasis, tumor, allergy, autoimmunity, allograft transplantation and control of microbial infection. Recently, Treg cell are isolated and can be expanded in vitro and in vivo, and their role is the subject of intensive investigation, particularly on the possible Treg cell therapy for various immune-mediated diseases. A growing body of evidence has demonstrated that Treg cells can prevent or even cure a wide range of diseases, including tumor, allergic and autoimmune diseases, transplant rejection, graft-versus-host disease. Currently, a large body of data in the literature has been emerging and provided evidence that clear understanding of Treg cell work will present definite opportunities for successful Treg cell immunotherapy for the treatment of a broad spectrum of diseases. In this Review, I briefly discuss the biology of Treg cells, and summarize efforts to exploit Treg cell therapy for autoimmune diseases. This article also explores recent observations on pharmaceutical agents that abrogate or enhance the function of Treg cells for manipulation of Treg cells for therapeutic purpose.