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DOI 10.3892/mmr.2017.6693

Медицинская библиотека · Molecular medicine reports · 2017

Potential role of autophagy in T‑cell survival in polymyositis and dermatomyositis.

Shu Xiaoming, Chen Fang, Peng Qinglin, Lu Xin, Tian Xiaolan, Wang Yan, Wang Guochun

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Аннотация

Peripheral blood T lymphocytopenia has previously been identified in polymyositis/dermatomyositis (PM/DM) patients. Therefore, the present study aimed to examine the potential role of autophagy in peripheral blood T cell survival in PM/DM patients. Transmission electron microscopy was used to detect the formation of autophagosomes of peripheral blood cluster of differentiation (CD)3+ T cells obtained from 24 patients with PM/DM and 21 healthy controls. Protein and mRNA expression levels of autophagy‑related molecules were examined by western blot analysis and reverse transcription‑quantitative polymerase chain reaction, respectively. The number of peripheral blood CD3+ T cells decreased significantly in PM/DM patients. The median percentage of apoptosis of CD3+ T cells in PM/DM patients was significantly increased compared with healthy controls. Furthermore, the number of autophagosomes and the expression of the autophagy markers microtubule‑associated protein 1A/1B‑light chain 3 (LC3) and Beclin‑1 were significantly reduced in the circulating CD3+ T cells of PM/DM patients compared with those of healthy controls. LC3 and Beclin‑1 protein levels correlated negatively with apoptosis rates in circulating CD3+ T cells in patients with PM/DM. CD3+ T cells from PM/DM patients treated with rapamycin increased autophagy and decreased apoptosis compared with untreated cells (P<0.05). In conclusion, these results suggested that autophagy may serve a potential protective role in the peripheral blood T cells of patients with PM/DM.

Для цитирования: Shu Xiaoming, Chen Fang, Peng Qinglin, Lu Xin, Tian Xiaolan, Wang Yan, Wang Guochun. Potential role of autophagy in T‑cell survival in polymyositis and dermatomyositis.. Molecular medicine reports. 2017. DOI: 10.3892/mmr.2017.6693.

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