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      • KCI등재

        Predictors of associated and multiple autoimmunity in children and adolescents with type 1 diabetes mellitus

        Kakleas Konstantinos,Kossyva Lydia,Korona Anastasia,Kafassi Nikolitsa,Karanasios Spyridon,Karavanaki Kyriaki 대한소아내분비학회 2022 Annals of Pediatirc Endocrinology & Metabolism Vol.27 No.3

        Purpose: Type 1 diabetes mellitus (T1DM) is an autoimmune condition characterised by the presence of antipancreatic antibodies. The autoimmune process is also directed against other organs, most frequently against the thyroid gland, intestinal mucosa, and gastric parietal cells. Methods: Our investigation included 121 children with T1DM with a mean age±standard deviation of 11.99±4.63 years (range, 2.0–20.0 years). We explored the frequency of associated autoimmunity; the presence of predictive factors such as current age, sex, and severity at diabetes diagnosis; T1DM duration; and family history of autoimmunity. Results: Associated autoimmunity was present in 28.9% of T1DM patients. Children with associated autoimmunity were older at diabetes diagnosis (P=0.009) and had a longer diabetes duration compared to children without associated autoimmunity (P=0.044). Adolescents aged 12–20 years had a statistically significant higher chance of developing thyroid autoimmunity compared to children aged 1–5 years (P=0.019). Multiple autoimmunity (MA), T1DM, and 2 or more autoimmune diseases were present in 5.8% of the study population. All children with MA presented with ketoacidosis at diabetes diagnosis and had a higher percentage of familial autoimmunity (P=0.042). The familial autoimmunity of these patients most frequently affected ≥3 relatives (P=0.026) and was more frequently diagnosed before 5 years of age (P=not significant). Conclusion: Associated autoimmunity was present in almost one-third of T1DM patients. Significant associations with associated autoimmunity were longer diabetes duration, female sex, older age at diabetes diagnosis, and glutamic acid decarboxylase positivity. Predictors of MA were age <5 years at T1DM diagnosis, the presence of diabetic ketoacidosis at diagnosis, and a significant family history of autoimmunity.

      • KCI등재

        Engineering Cell Therapies for Autoimmune Diseases: From Preclinical to Clinical Proof of Concept

        Oh Sangwook,Payne Aimee S. 대한면역학회 2022 Immune Network Vol.22 No.5

        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.

      • KCI등재

        Autoimmune Responses in Severe Asthma

        Manali Mukherjee,Parameswaran Nair 대한천식알레르기학회 2018 Allergy, Asthma & Immunology Research Vol.10 No.5

        Asthma and autoimmune diseases both result from a dysregulated immune system, and have been conventionally considered to have mutually exclusive pathogenesis. Autoimmunity is believed to be an exaggerated Th1 response, while asthma with a Th2 underpinning is congruent with the well-accepted Th1/Th2 paradigm. The hypothesis of autoimmune involvement in asthma has received much recent interest, particularly in the adult late-onset non-atopic patients (the “intrinsic asthma”). Over the past decades, circulating autoantibodies against diverse self-targets (beta-2-adrenergic receptors, epithelial antigens, nuclear antigens, etc.) have been reported and subsequently dismissed to be epiphenomena resulting from a chronic inflammatory condition, primarily due to lack of evidence of causality/pathomechanism. Recent evidence of ‘granulomas’ in the lung biopsies of severe asthmatics, detection of pathogenic sputum autoantibodies against autologous eosinophil proteins (e.g., eosinophil peroxidase) and inadequate response to monoclonal antibody therapies (e.g., subcutaneous mepolizumab) in patients with evidence of airway autoantibodies suggest that the role of autoimmune mechanisms be revisited. In this review, we have gathered available reports of autoimmune responses in the lungs, reviewed the evidence in the context of immunogenic tissue-response and danger-associated molecular patterns, and constructed the possibility of an autoimmune-associated pathomechanism that may contribute to the severity of asthma.

      • Review : Regulation of nuclear factor-kB in autoimmunity

        ( Shao Cong Sun ),( Jae Hoon Chang ),( Jin Jin ) 영남대학교 약품개발연구소 2013 영남대학교 약품개발연구소 연구업적집 Vol.23 No.0

        Nuclear factor (NF)-kB transcripition factors are pivotal regulators of innate and adaptive immune responses, and perturbations of NF- kB signaling contribute to the pathogenesis of immunological disorders. NF-kB is a well-known proinflammatory mediator, and its deregu-lated activation is associated with the chronic inflamma-tion of autoimmune diseases. Paradoxically, NF-kB plays a crucial role in the establishment of immune tolerance including both central tolerance and the peripheral func-ton of regulatory T (Treg) cells. Thus, defective or deregulated activation of NF-kB may contribute to au-toimmunity and inflammation, highlighting the impor-tance of tightly controlled NF-kB signaling. This review focuses on recent progress regarding NF-kB regulation and its association with autoimmunity.

      • KCI등재

        Gut microbiota in autoimmunity: potential for clinical applications

        김동현,유승아,김완욱 대한약학회 2016 Archives of Pharmacal Research Vol.39 No.11

        Microbial habitation in the human body beginsimmediately after birth, and adults are colonized bymicrobes outnumbering human cells by a factor of ten. Especially, intestinal track is a living space for diversemicrobial species that have coevolved symbiotically. Aprincipal function of the gut microbiota is to protect thehost from harmful bacteria and to provide benefits for thehost through several mechanisms, including direct com-petition for limited nutrients, training of host immunesystems to recognize specifically foreign materials andconversion of otherwise indigestible food into energy andabsorbable nutrients. Therefore, gut dysbiosis, a bacterialimbalance state, is related with the pathogenesis of varioushost diseases including autoimmune diseases. In the currentreview, we highlight the importance of gut microbiota inthe normal health and autoimmune diseases. We also dis-cuss regulation of gut dysbiosis and future direction forpotential clinical applications, including treatment anddiagnostics of autoimmune diseases.

      • KCI등재

        Cytokines, Vascular Endothelial Growth Factors, and PlGF in Autoimmunity: Insights From Rheumatoid Arthritis to Multiple Sclerosis

        Lee Young eun,Lee Seung-Hyo,Kim Wan-Uk 대한면역학회 2024 Immune Network Vol.24 No.1

        In this review, we will explore the intricate roles of cytokines and vascular endothelial growth factors in autoimmune diseases (ADs), with a particular focus on rheumatoid arthritis (RA) and multiple sclerosis (MS). AD is characterized by self-destructive immune responses due to auto-reactive T lymphocytes and Abs. Among various types of ADs, RA and MS possess inflammation as a central role but in different sites of the patients. Other common aspects among these two ADs are their chronicity and relapsing-remitting symptoms requiring continuous management. First factor inducing these ADs are cytokines, such as IL-6, TNF-α, and IL-17, which play significant roles in the pathogenesis by contributing to inflammation, immune cell activation, and tissue damage. Secondly, vascular endothelial growth factors, including VEGF and angiopoietins, are crucial in promoting angiogenesis and inflammation in these two ADs. Finally, placental growth factor (PlGF), an emerging factor with bi-directional roles in angiogenesis and T cell differentiation, as we introduce as an "angio-lymphokine" is another key factor in ADs. Thus, while angiogenesis recruits more inflammatory cells into the peripheral sites, cytokines secreted by effector cells play critical roles in the pathogenesis of ADs. Various therapeutic interventions targeting these soluble molecules have shown promise in managing autoimmune pathogenic conditions. However, delicate interplay between cytokines, angiogenic factors, and PlGF has more to be studied when considering their complementary role in actual pathogenic conditions. Understanding the complex interactions among these factors provides valuable insights for the development of innovative therapies for RA and MS, offering hope for improved patient outcomes.

      • KCI등재

        CD4+CD25+ Regulatory T Cells Selectively Diminish Systemic Autoreactivity in Arthritic K/BxN Mice

        Sang Mee Kang,장은경,백두진,장영주,윤지희 한국분자세포생물학회 2008 Molecules and cells Vol.25 No.1

        Although the arthritis symptoms observed in the K/BxN model have been shown to be dependent on the functions of T and B cells specific to the self antigen glucose-6-phosphate isomerase, less is known about the in vivo roles of CD4+CD25+ regulatory T (Treg) cells in the pathology of K/BxN mice. We determined the quantitative and functional characteristics of the Treg cells in K/BxN mice. These mice contained a higher percentage of Foxp3+ Treg cells among the CD4+ T cells than their BxN littermates. These Treg cells were anergic and efficiently suppressed the proliferation of naïve CD4+ T cells and cytokine production by effector CD4+ T cells in vitro. Antibody-mediated depletion of CD25+ cells caused K/BxN mice to develop multi-organ inflammation and autoantibody production, while the symptoms of arthritis were not affected. These results demonstrate that despite the inability of the Treg cells to suppress arthritis development, they play a critical role protecting the arthritic mice from systemic expansion of autoimmunity.

      • KCI등재SCISCIE

        CD4<sup>+</sup>CD25<sup>+</sup> Regulatory T Cells Selectively Diminish Systemic Autoreactivity in Arthritic K/BxN Mice

        Kang, Sang mee,Jang, Eun kyeong,Paik, Doo jin,Jang, Young ju,Youn, Jee hee Korean Society for Molecular Biology 2008 Molecules and cells Vol.25 No.1

        Although the arthritis symptoms observed in the K/BxN model have been shown to be dependent on the functions of T and B cells specific to the self antigen glucose-6-phosphate isomerase, less is known about the in vivo roles of CD4<sup>+</sup>CD25<sup>+</sup> regulatory T (T<sub>reg</sub> ) cells in the pathology of K/BxN mice. We determined the quantitative and functional characteristics of the T<sub>reg</sub> cells in K/BxN mice. These mice contained a higher percentage of Foxp3<sup>+</sup> T<sub>reg</sub> cells among the CD4<sup>+</sup> T cells than their BxN littermates. These T<sub>reg</sub> cells were anergic and efficiently suppressed the proliferation of naive CD4<sup>+</sup> T cells and cytokine production by effector CD4<sup>+</sup> T cells in vitro. Antibody-mediated depletion of CD25<sup>+</sup> cells caused K/BxN mice to develop multi-organ inflammation and autoantibody production, while the symptoms of arthritis were not affected. These results demonstrate that despite the inability of the T<sub>reg</sub> cells to suppress arthritis development, they play a critical role protecting the arthritic mice from systemic expansion of autoimmunity.

      • KCI등재

        Autoimmune Gastritis Accompanied by a Schwannoma Presenting as a Subepithelial Tumor

        Yong Hwan Ahn,Kyo Bum Hwang,Geom Seog Seo 대한상부위장관ㆍ헬리코박터학회 2023 Korean Journal of Helicobacter Upper Gastrointesti Vol.23 No.2

        Autoimmune gastritis (AIG), a chronic inflammatory disease occurs as a result of a complex interaction between host-related and environmental factors. AIG may progress to severe atrophic gastritis secondary autoimmune-mediated parietal cell destruction in the stomach. AIG can be diagnosed based on anti-parietal cell antibody tests and endoscopy, which reveals widespread gastric corpus atrophy in patients with low serum pepsinogen I levels, a low pepsinogen I/II ratio, and elevated serum gastrin levels on serological testing. Tissue biopsy findings, which include mucosal atrophy and lymphocytic infiltration of the lamina propria may be useful for diagnostic confirmation. Decreased gastric acid secretion causes hypergastrinemia and enterochromaffin-like (ECL) cell proliferation, which can lead to neuroendocrine tumor development. Additionally, an autoimmune response results in parietal and chief cell injury, and proliferating ECL cells are detected in the deep mucosal layers in patients with AIG. Therefore, this condition may easily be misdiagnosed as a subepithelial tumor, and establishing a differential diagnosis for other types of subepithelial tumor accompanied by AIG is challenging. We present the case of a 54-year-old woman who was diagnosed with AIG with a concomitant subepithelial tumor based on serologic tests and biopsy findings and underwent wedge resection, which confirmed diagnosis of a schwannoma.

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