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Abstract Number: 1943

Autophagy Expressions Were Decreased in Circulating T Cells in Inflammatory Myopathies Patients

Fang Chen1, Xiaoming Shu2, Xin Lu3 and Guochun Wang1, 1Department of Rheumatology, China-Japan Friendship Hospital, Beijing, China, 2China-Japan Friendship Hospital, Beijing, China, 3Rheumatology, China-Japan Friendship Hospital, Beijing, China

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: T cells and myositis

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Session Information

Title: Muscle Biology, Myositis and Myopathies: Genetics, Autoantibodies and other Molecular Aspects of Idiopathic Inflammatory Myopathies and Models

Session Type: Abstract Submissions (ACR)

Background/Purpose: The autophagy in circulating lymphocytes in IIM patients has not been clarified yet. Our research is aimed to study the autophagy in circulating T cells in IIM patients and to explore the possible role of aberrant autophagy contributing to the pathogenesis of IIM.

Methods: circulating T cells were isolated from 27 IIM patients and 19 normal controls. The expressions of protein and mRNA level of autophagy-related molecules (LC3, Beclin1) were examined by western blot and quantitative PCR. Transmission electron microscope was applied to detect the formation of autophagosome in circulating T cells.  

Results: The formation of autohagosome in circuiting T cells of IIM patients was decreased than those of normal controls (P<0.01).  the expression of LC3 and Beclin1 proteins and mRNA level in circulating T cells of IIM patients( Beclin protein: 0.34±0.08; LC3 protein: 0.08±0.03 ; Beclin mRNA: 0.014±0.007; LC3 mRNA: 0.11±0.046) were both significantly lower in IIM patients than those in healthy controls( Beclin protein: 0.52±0.13 ;LC3 prorein: 0.13±0.05; Beclin mRNA:0.021±0.01 ;LC3 m RNA : 0.17±0.095 ) ( all p<0.05).

Conclusion: Autophagy expression was decreased in circulating T cells in IIM patients. Further study is needed to explore the possible role of aberrant autophagy contributing to the pathogenesis of IIM�B


Disclosure:

F. Chen,
None;

X. Shu,
None;

X. Lu,
None;

G. Wang,
None.

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