• 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.

• The Journal of Korean Medicine
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• v.25 no.4
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• pp.188-199
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• 2004

Transglutaminase 2 (TGase 2) is an enzyme that is widely used in many biological systems for generic tissue stabilization purposes or immediate defenses for wounds. Many reports have showed that TGase 2 is aberrantly activated in tissues and cells and contributes to a variety of diseases, including neurodegenerative diseases and autoimmune diseases. In most cases, the TGase 2 appears to be a factor in the formation of inappropriate proteinaceous aggregates that may be cytotoxic. However, in other cases such as celiac disease, arthritis, lupus, amyotrophic lateral sclerosis, TGase 2 is involved in the generation of autoantibodies. This suggests the possibility that the inappropriate expression and/or presentation of TGase 2 to T cells might contribute to these diseases in genetically predisposed individuals. Others and we have found that TGase 2 expression is also increased in the inflammation process. We also demonstrated reverse of inflammation by TGase inhibition. Furthermore we discovered the genuine role of TGase 2 in immune cell activation. Increase of TGase activity induces or exacerbates inflammation via NF-κB activation without I-κBα kinase signalings. This review will examine a possibility of TGase inhibitors as therapeutic agents in a variety of inflammatory diseases.

• IMMUNE NETWORK
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• v.22 no.1
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• pp.7.1-7.20
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• 2022

Recently, there have been impressive advancements in understanding of the immune mechanisms underlying cutaneous inflammatory diseases. To understand these diseases on a deeper level and clarify the therapeutic targets more precisely, numerous studies including in vitro experiments, animal models, and clinical trials have been conducted. This has resulted in a paradigm shift from non-specific suppression of the immune system to selective, targeted immunotherapies. These approaches target the molecular pathways and cytokines responsible for generating inflammatory conditions and reinforcing feedback mechanisms to aggravate inflammation. Among the numerous types of skin inflammation, psoriasis and atopic dermatitis (AD) are common chronic cutaneous inflammatory diseases. Psoriasis is a IL-17-mediated disease driven by IL-23, while AD is predominantly mediated by Th2 immunity. Autoimmune bullous diseases are autoantibody-mediated blistering disorders, including pemphigus and bullous pemphigoid. Alopecia areata is an organ-specific autoimmune disease mediated by CD8⁺ T-cells that targets hair follicles. This review will give an updated, comprehensive summary of the pathophysiology and immune mechanisms of inflammatory skin diseases. Moreover, the therapeutic potential of current and upcoming immunotherapies will be discussed.

• Proceedings of the Korean Society of Veterinary Clinics Conference
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• 2006.11a
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• pp.198-202
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• 2006

• 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-A^q in a murine CIA model. We found that recombinant I-A^q/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-A^q/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.

• IMMUNE NETWORK
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• v.24 no.2
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• pp.12.1-12.17
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• 2024

Exosomes are double phospholipid membrane vesicles that are synthesized and secreted by a variety of cells, including T cells, B cells, dendritic cells, immune cells, are extracellular vesicles. Recent studies have revealed that exosomes can play a significant role in under both physiological and pathological conditions. They have been implicated in regulation of inflammatory responses, immune response, angiogenesis, tissue repair, and antioxidant activities, particularly in modulating immunity in autoimmune diseases (AIDs). Moreover, variations in the expression of exosome-related substances, such as miRNA and proteins, may not only offer valuable perspectives for the early warning, and prognostic assessment of various AIDs, but may also serve as novel markers for disease diagnosis. This article examines the impact of exosomes on the development of AIDs and explores their potential for therapeutic application.

• IMMUNE NETWORK
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• v.10 no.3
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• pp.81-84
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• 2010

B cells, by virtue of their diverse roles in immune responses to foreign and self antigens, have become of increasing interest to the clinician as well as the basic immunologist. In particular, it is now apparent that the development of B cell unresponsiveness in antibody and T cell mediated autoimmune disorders and the transplant setting is both worthwhile and achievable.

• Neonatal Medicine
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• v.28 no.3
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• pp.139-142
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• 2021

Macrophage activation syndrome (MAS) is a potentially life-threatening complication in many autoimmune diseases. Early recognition and intervention are essential for a favorable outcome. Neonatal lupus, an acquired autoimmune disease in neonates caused by the transplacental passage of maternal autoantibodies, is rare and usually self-limited. Herein, we report a case of MAS in a patient with neonatal lupus, which improved with intravenous immunoglobulin.

• 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.

• Toxicological Research
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• v.23 no.2
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• pp.97-105
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• 2007

Toll-like receptors (TLRs) playa crucial role in initiating and regulating innate and adaptive immune responses by detecting invading microbial pathogens. TLRs can also respond to non-microbial molecules derived from damaged tissue. Accumulating evidence suggests that deregulation of TLRs results in the dysfunction of immune system and ultimately increases the risk of many immune and inflammatory diseases including infectious diseases, allergy, and autoimmune diseases. Therefore, understanding how the immune system is controlled by TLRs will provide new insight to find the way to prevent or treat infectious diseases and immune disorders.