کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6087407 1207362 2014 14 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Class I and II histone deacetylase inhibition by ITF2357 reduces SLE pathogenesis in vivo
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ایمونولوژی
پیش نمایش صفحه اول مقاله
Class I and II histone deacetylase inhibition by ITF2357 reduces SLE pathogenesis in vivo
چکیده انگلیسی


- Lupus-prone NZB/W mice were treated with a class I/II HDACi (ITF2357).
- ITF2357 treatment decreases anti-nuclear antibodies and immune complex deposition.
- ITF2357 treatment increases the Treg phenotype and Foxp3 acetylation.
- HDAC inhibition decreases SLE in NZB/W mice by altering the T cell phenotype.

We sought to determine if a specific class I and II HDAC inhibitor (ITF2357) was able to decrease disease in lupus-prone NZB/W mice through regulation of T cell profiles. From 22 to 38 weeks-of-age, NZB/W and non-lupus NZW mice were treated with ITF2357 (5 mg/kg or 10 mg/kg), or vehicle control. Body weight and proteinuria were measured every 2 weeks, while sera anti-dsDNA and cytokine levels were measured every 4 weeks. Kidney disease was determined by sera IgG levels, immune complex deposition, and renal pathology. T lymphocyte profiles were assessed using flow cytometric analyses. Our results showed that NZB/W mice treated with the 10mg/kgof ITF2357 had decreased renal disease and inflammatory cytokines in the sera. Treatment with ITF2357 decreased the Th17 phenotype while increasing the percentage of Tregs as well as Foxp3 acetylation. These results suggest that specific HDAC inhibition may decrease disease by altering T cell differentiation and acetylation.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Clinical Immunology - Volume 151, Issue 1, March 2014, Pages 29-42
نویسندگان
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