• IMMUNE NETWORK
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• v.11 no.5
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• pp.227-244
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• 2011

MicroRNAs (miRNAs) are small noncoding RNA molecules that negatively regulate gene expression via degradation or translational repression of their target messenger RNAs (mRNAs). Recent studies have clearly demonstrated that miRNAs play critical roles in several biologic processes, including cell cycle, differentiation, cell development, cell growth, and apoptosis and that miRNAs are highly expressed in regulatory T (Treg) cells and a wide range of miRNAs are involved in the regulation of immunity and in the prevention of autoimmunity. It has been increasingly reported that miRNAs are associated with various human diseases like autoimmune disease, skin disease, neurological disease and psychiatric disease. Recently, the identification of miRNAs in skin has added a new dimension in the regulatory network and attracted significant interest in this novel layer of gene regulation. Although miRNA research in the field of dermatology is still relatively new, miRNAs have been the subject of much dermatological interest in skin morphogenesis and in regulating angiogenesis. In addition, miRNAs are moving rapidly center stage as key regulators of neuronal development and function in addition to important contributions to neurodegenerative disorder. Moreover, there is now compelling evidence that dysregulation of miRNA networks is implicated in the development and onset of human neruodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, Huntington's disease, Tourette's syndrome, Down syndrome, depression and schizophrenia. In this review, I briefly summarize the current studies about the roles of miRNAs in various autoimmune diseases, skin diseases, psychoneurological disorders and mental stress.

• IMMUNE NETWORK
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• v.2 no.2
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• pp.79-85
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• 2002

Background: In contrast to evidences of Ig H chain receptor editing in transformed cell lines and transgenic mouse models, there has been no direct evidence that this phenomenon occurs in human developing B cells. Methods: $V_HDJ_H$ rearrangements were obtained from genomic DNA of individual $IgM^-$ B cells from liver and $IgM^+B$ cells from bone marrow of 18 wk of gestation human fetus by PCR amplification and direct sequencing. Results: We found three examples of H chain receptor editing from $IgM^+$ and $IgM^-human$ fetal B cells. Two types of $V_H$ replacements were identified. The first involved $V_H$ hybrid formation, in which part of a $V_H$ gene from the initial VDJ rearrangement is replaced by part of an upstream $V_H$ gene at the site of cryptic RSS. The second involved a gene conversion like replacement of CDR2, in which another $V_H$ gene donated a portion of its CDR2 sequence to the initial VDJ rearrangement. Conclusion: These data provide evidence of receptor editing at the H chain loci in developing human B cells, and also the first evidence of a gene conversion event in human Ig genes.

• BMB Reports
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• v.51 no.8
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• pp.371-372
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• 2018

Cardiovascular disease such as atherosclerosis is caused by imbalanced lipid metabolism and represents a leading cause of death worldwide. Epidemiological studies show that patients with systemic autoimmune diseases exhibit a higher incidence of atherosclerosis. Conversely, hyperlipidemia has been known to accelerate the incidence of autoimmune diseases in humans and in animal models. However, there is a considerable gap in our understanding of how atherosclerosis impacts the development of the autoimmunity in humans, and vice versa. The atherosclerosis-related autoimmune diseases include psoriasis, rheumatoid arthritis, systemic lupus erythematosus (SLE) and diabetes mellitus. By using animal models of atherosclerosis and SLE, we have recently demonstrated that hyperlipidemia significantly accelerates the development of autoantibodies, by inducing autoimmune follicular helper T ($T_{FH}$) cells. Mechanistic studies have identified that hyperlipidemia induces IL-27 production in a TLR4-dependent manner, likely via downregulating LXR expression in dendritic cells. In this case, mice lacking IL-27 do not develop enhanced antibody responses. Thus it is noted that these findings propose a mechanistic insight responsible for the tight association between cardiovascular diseases and SLE in humans.

• IMMUNE NETWORK
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• v.14 no.1
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• pp.7-13
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• 2014

Molecular mimicry is an attractive mechanism for triggering autoimmunity. In this review, we explore the potential role of evolutionary conserved bacterial proteins in the production of autoantibodies with focus on granulomatosis with polyangiitis (GPA) and rheumatoid arthritis (RA). Seven autoantigens characterized in GPA and RA were BLASTed against a bacterial protein database. Of the seven autoantigens, proteinase 3, type II collagen, binding immunoglobulin protein, glucose-6-phosphate isomerase, ${\alpha}$-enolase, and heterogeneous nuclear ribonuclear protein have well-conserved bacterial orthologs. Importantly, those bacterial orthologs are also found in human-associated bacteria. The wide distribution of the highly conserved stress proteins or enzymes among the members of the normal flora and common infectious microorganisms raises a new question on how cross-reactive autoantibodies are not produced during the immune response to these bacteria in most healthy people. Understanding the mechanisms that deselect auto-reactive B cell clones during the germinal center reaction to homologous foreign antigens may provide a novel strategy to treat autoimmune diseases.

• Natural Product Sciences
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• v.17 no.4
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• pp.354-362
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• 2011

Systemic lupus erythematosus (SLE) is a systemic inflammatory autoimmune disease characterized by abnormalities in T cell immunoregulation and hyperreactivity of B cells, leading to autoantibody production and multiorgan injuries. We investigated the effect of baicalin on aberrant immunoregulation in pristane-induced lupus mice. Mice received i.p. a single injection of 0.5 ml of pristane or PBS, and approximately 3 months later, were used as a pristane-induced lupus model or healthy controls. The pristane-induced lupus mice and healthy mice were randomly divided into three groups: healthy mouse group (healthy control), pristane-primed lupus control group (lupus control), and baicalin (BAC)-treated pristane-primed lupus mouse group (BAC-treated lupus). The pristane-induced lupus mice and healthy mice were administrated orally with BAC 50 mg/kg or PBS once in a day for 10 ds. These results demonstrated that levels of serum IL-6, LPS-induced production of IL-6, $PGE_2$ and NO by macrophages, $PGE_2$-stimulated production of IL-6 by macrophages and IFN-${\gamma}$ by thymocytes, and an overexpression of splenic NKT cells and CD69+CD4+ T cells were downregulated in BAC-treated lupus compared to lupus control, while reduced apoptosis of splenic CD4+ T cells were upregulated. Therefore, these findings suggest that BAC may attenuate autoimmunity and disease activity in lupus via downregulation of aberrant activation of T cells and inhibition of overproduction of IL-6 and $PGE_2$ in pristane-induced lupus mice.

• Korean Journal of Microbiology
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• v.43 no.4
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• pp.237-242
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• 2007

One of the chief characteristics of the retrovirus life cycle is the appearance of provirus caused by integration of viral genome into the host cell genome, and its delivery stably to the next generation as a part of host germ line. This stable form is called endogenous retrovirus (ERV) and expressed by exogenous or endogenous factors. HERVs and MuERVs are present in humans and mice correspondingly, and their expressions frequently cause diseases. Several diseases such as cancer, autoimmunity and neurological disorders are related with HERVs. Therefore, various strategies should be established for the development of effective therapies for the suffering patients.

• Clinical and Experimental Pediatrics
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• v.45 no.9
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• pp.1165-1169
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• 2002

Satoyoshi syndrome(generalized Komuragaeri disease) is a rare disorder of unknown cause, characterized by progressive, painful, intermittent muscle spasms and alopecia. Endocrinopathy with amenorrhea, secondary skeletal abnormalities, and diarrhea or unusual malabsorption are frequently seen. It seems that autoimmunity may play a role in its pathogenesis. We report a 13-year-old girl with characteristic manifestations of the syndrome. She was treated with intravenous gammaglobulin and Prednisolone. Painful muscle cramps were gradually improved, but the scalp condition did not change. Satoyoshi syndrome should be considered in children with unexplained muscle spasms and alopecia.

• The Journal of the Korea institute of electronic communication sciences
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• v.3 no.4
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• pp.233-239
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• 2008

This study is study regarding system implementation that a ruler maximizing an autoimmunity effect supported it as I stimulate I am visual hearing so that treatment ability is possible. As I am known in a lot of conspiracy mental problems by being disproportionate for a direct reason to be connected to an action, the brain whom emotional, govern spirits through fragrance to stimulate sense of smell so that, specially, an ARoMa treatment is effective. I will inquire into changes and an influence around alpha of the rear wave object before watching this system.

• Korean Journal of Veterinary Research
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• v.56 no.2
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• pp.117-120
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• 2016

Experimental autoimmune encephalomyelitis (EAE) in Lewis rats is characterized by transient paralysis followed by recovery. To evaluate whether transient paralysis in EAE affects bone density, tibiae of EAE rats were morphologically investigated using micro-computed tomography and histology. The parameters of bone health were significantly reduced at the peak stage of EAE rats relative to those of controls (p < 0.05). The reduction of bone density was found to remain unchanged, even in the recovery stage. Collectively, the present data suggest that osteoporosis occurs in paralytic rats with monophasic EAE, possibly through the disuse of hindlimbs and/or autoimmune inflammation.

• Archives of Pharmacal Research
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• v.28 no.3
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• pp.274-279
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• 2005

Pharmacological inhibition of interleukin-12 (IL-12) production may be a therapeutic strategy for preventing the development and progression of disease in experimental models of autoimmunity. In this study, the effects of myricetin, a naturally occurring flavonoid present in fruits, vegetables and medicinal herbs, on the production of IL-12 were investigated in mouse macrophages stimulated with lipopolysaccharide (LPS). Myricetin significantly inhibited the LPS­induced IL-12 production from both primary macrophages and the RAW264.7 monocytic cell-line in a dose-dependent manner. The effect of myricetin on IL-12 gene promoter activation was analyzed by transfecting RAW264.7 cells with IL-12 gene promoter/luciferase constructs. The repressive effect was mapped to a region in the IL-12 gene promoter containing a binding site for NF-${\kappa}B$. Furthermore, activation of macrophages by LPS resulted in markedly enhanced binding activity to the NF-${\kappa}B$ site, which significantly decreased upon addition of myricetin, indicating that myricetin inhibited IL-12 production in LPS-activated macrophages via the down­regulation of NF-KB binding activity.