Low expression of human histocompatibility leukocyte antigen-DR is associated with hypermethylation of human histocompatibility leukocyte antigen-DR alpha gene regions in B cells from patients with systemic lupus erythematosus.

Sano, Hiroshi; Compton, Lara; Shiomi, Norio; Steinberg, A D; Jackson, Richard A.; Sasaki, Takeshi

doi:10.1172/jci112105

Cited by 26 publications

(17 citation statements)

References 56 publications

(48 reference statements)

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“…9B). Furthermore, these results, by suggesting that RFX1 recruits DNMT1 to specific genomic loci, shed light on a mechanistic underpinning for the coexistence of both hypomethylated genes, including CD11a [7], CD70 [8], CD40 ligand [30] and perforin [50]; and hypermethylated genes, such as the HLA-DR alpha gene in lupus [51].…”

Section: Discussionmentioning

confidence: 83%

Epigenetics and SLE: RFX1 downregulation causes CD11a and CD70 overexpression by altering epigenetic modifications in lupus CD4+ T cells

Zhao¹,

Sun²,

Gao³

et al. 2010

Journal of Autoimmunity

139

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Section: Discussionmentioning

confidence: 83%

Epigenetics and SLE: RFX1 downregulation causes CD11a and CD70 overexpression by altering epigenetic modifications in lupus CD4+ T cells

Zhao¹,

Sun²,

Gao³

et al. 2010

Journal of Autoimmunity

139

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“…This may be another contributing factor to the development of the disease in the AE°DQ2 mice. In fact, the decreased level of MHC class II expression is reported in active SLE and other immune diseases 47–50. Nonetheless, the age-control AE° (null) mice with virtually no class II molecule do not develop lupus-like disease (data not shown).…”

Section: Discussionmentioning

confidence: 83%

Spontaneous lupus-like syndrome in HLA-DQ2 transgenic mice with a mixed genetic background

Rashtak

Marietta

Cheng

et al. 2010

Lupus

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To investigate the role of HLA-DQ2 in the pathogenesis of associated immune disorders, we generated transgenic mice that expressed HLA-DQ2 in the absence of endogenous murine class II molecules (AE°DQ2). These AE°DQ2 mice with a mixed genetic background spontaneously developed skin lesions on their ears, whereas control AE°DQ6 genotype control mice (also with a mixed genetic background) did not. The skin lesions were characterized by deep subepidermal blistering with hydropic degeneration and lymphoid infiltration in the subepidermal area as determined by histopathology. Immunofluorescence analysis revealed thick band-like granular deposition of IgG, IgM, and a thin band of IgA deposition along the basement membrane. AE°DQ2 mice also developed significant and progressive hematuria and proteinuria as compared to the AE°DQ6 mice (P<0.05). Histopathology showed immune complex deposits in the glomeruli of AE°DQ2 mice. Immunofluorescence analysis showed progressive mesangial and capillary wall deposition of IgA, IgM, IgG and C1q in the kidney. With electron microscopy, the deposits showed a “fingerprint” substructure; and tubuloreticular structures were identified within endothelial cells. Conversely, these changes were not observed in AE°DQ6 mice. Serum anti-dsDNA IgM and IgG levels were also significantly elevated among AE°DQ2 mice compared to AE°DQ6 mice (P<0.001). In conclusion, AE°DQ2 mice spontaneously develop an autoimmune lupus-like syndrome and are useful model for this disease. It remains to be determined whether genetic admixture played a role in the development of this SLE-like syndrome in HLA-DQ2 transgenic mice.

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“…верхности [44], а также в отношение апоптоти-ческого гена DR3 в синовиальных клетках при ревматоидном артрите, что может обуславли-вать резистентность последних к апоптозу [52]. Гиперметилирование, а, следовательно, и «мол-чание» гена IL-10, мощного противовоспали-тельного цитокина, было обнаружено в клетках периферической крови больных РА.…”

Section: клеточный геном в патогенезе основных заболеваний 2010 т 1unclassified

Cellular Genome in Pathogenesis of Basic Diseases in Humans (Atherosclerosis, Autoimmune Diseases, Cancer)

Козлов¹

2014

Med.Imm.Rus

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Трудно, нет, невозможно себе представить то количество заболеваний, которые приносят страдания современному человеку. Не счесть алмазов… Среди этого «алмазного» множества все же можно обозначить основные заболевания с точки зрения их ведущего, основополагающего значения в причинах смертности современного жителя планеты Земля: это атеросклероз, это рак, это аутоиммунные и отдельные инфекцион-ные заболевания. И что самое главное, мы еще ох как очень далеки от окончательного решения проблем этиопатогенеза и терапии этих заболе-ваний. Естественно, что эти группы основных Адрес для переписки:Козлов Владимир Александрович, 630090, г. Новосибирск, ул. Ядринцевская, 14. Тел.: (383) 222-66-27. Факс: (383) 222-70-28. E-mail: v_kozlov@online.nsk.su КЛЕТОЧНЫЙ ГЕНОМ В ПАТОГЕНЕЗЕ ОСНОВНЫХ ЗАБОЛЕВАНИЙ ЧЕЛОВЕКА (АТЕРОСКЛЕРОЗ, АУТОИММУННЫЕ ЗАБОЛЕВАНИЯ, РАК)Козлов В.А. НИИ клинической иммунологии СО РАМН, г. НовосибирскРезюме. Несмотря на значительные различия в этиологии, патогенезе, клинико-лабораторных данных, наконец, различия в клиническом течении таких заболеваний, как атеросклероз, аутоим-мунные и аллергические заболевания накоплены данные, свидетельствующие о том, что в основе этих заболеваний имеется много общего. В первую очередь это касается механизмов эпигенетической регуляции экспрессии генов, характер изменений которой практически тождественен и проявляет-ся тотальным гипометилированием и возвратным гиперметилированием отдельных генов. Схожи-ми при этих патологиях являются также процессы, связанные с регуляцией длины теломер. Все это ставит вопрос о скорейшей разработке методов лечения данных патологий с помощью препаратов, влияющих на молекулярно-биохимические механизмы, лежащих в основе эпигенетической регуля-ции экспрессии генов.Ключевые слова : геном, метилирование, теломеры, атеросклероз, рак. Kozlov V.A. CELLULAR GENOME IN PATHOGENESIS OF BASIC DISEASES IN HUMANS (ATHEROSCLEROSIS, AUTOIMMUNE DISEASES, CANCER)Abstract. Despite of considerable differences in etiology, pathogenesis, clinical and laboratory, data, and, finally, different clinical features of such diseases as atherosclerosis, autoimmune and allergic diseases, there exists a lot of evidence suggesting that, basically, these disorders have much in common. First of all, it concerns epigenetic regulatory mechanisms of gene expression that show virtually identical patterns of changes, i.e., total hypomethylation and reversible hypermethylation of distinct genes. The events connected with regulation of telomere length are also similar in all the mentioned disorders. In general, this concept draws attention to current needs for urgent development of novel therapeutic approaches for these very common disorders, by means of drugs that would be able to influence some molecular mechanisms, underlying epigenetic regulation of gene expression. (Med. Immunol., vol. 12, N 4-5, pp 285-296)

show abstract

Low expression of human histocompatibility leukocyte antigen-DR is associated with hypermethylation of human histocompatibility leukocyte antigen-DR alpha gene regions in B cells from patients with systemic lupus erythematosus.

Abstract: The relationship between the expression of HLA-DR antigens and the HLA-DRct gene methylation was examined in systemic lupus erythematosus (SLE)

Cited by 26 publications

References 56 publications

Epigenetics and SLE: RFX1 downregulation causes CD11a and CD70 overexpression by altering epigenetic modifications in lupus CD4+ T cells

Epigenetics and SLE: RFX1 downregulation causes CD11a and CD70 overexpression by altering epigenetic modifications in lupus CD4+ T cells

Spontaneous lupus-like syndrome in HLA-DQ2 transgenic mice with a mixed genetic background

Cellular Genome in Pathogenesis of Basic Diseases in Humans (Atherosclerosis, Autoimmune Diseases, Cancer)

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