کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
6138490 1594219 2016 12 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Interferon-dependent immunoproteasome activity during mouse adenovirus type 1 infection
موضوعات مرتبط
علوم زیستی و بیوفناوری ایمنی شناسی و میکروب شناسی ویروس شناسی
پیش نمایش صفحه اول مقاله
Interferon-dependent immunoproteasome activity during mouse adenovirus type 1 infection
چکیده انگلیسی


- Mouse adenovirus type 1 (MAV-1) infection increased immunoproteasome (IP) activity.
- MAV-1-induced IP expression depended on IFN-γ.
- IP activity was not essential for control of MAV-1 replication.
- IP deficiency did not affect MAV-1-induced inflammation in heart or lung.

The immunoproteasome is an inducible host mechanism that aids in the clearance of damaged proteins. The immunoproteasome also influences immune function by enhancing peptide presentation by MHC class I and promotes inflammation via IκB degradation and activation of NF-κB. We used mouse adenovirus type 1 (MAV-1) to characterize the role of the immunoproteasome in adenovirus pathogenesis. Following intranasal infection of mice, immunoproteasome activity in the heart and lung was significantly increased in an IFN-γ-dependent manner. Absence of the β5i immunoproteasome subunit and pharmacological inhibition of β5i activity had minimal effects on viral replication, virus-induced cellular inflammation, or induction of cytokine expression. Likewise, the establishment of protective immunity following primary infection was not significantly altered by β5i deficiency. Thus, although immunoproteasome activity is robustly induced during acute infection with MAV-1, our data suggest that other mechanisms are capable of compensating for immunoproteasome activity to maintain antiviral immunity and appropriate inflammatory responses.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Virology - Volume 498, November 2016, Pages 57-68
نویسندگان
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