Ping Li
Wuhan University
12 Papers
36 Citations
Ping Li is an academic researcher from Wuhan University. The author has contributed to research in topics: Medicine & CD8. The author has an hindex of 7, co-authored 9 publications.
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Papers
Mesenchymal stem cells abrogate experimental asthma by altering dendritic cell function
TL;DR: The present study used a mouse model of asthma to demonstrate that transplantation of MSCs suppressed features of asthma by targeting the function of lung myeloid DCs, and supported that M SCs may be used as a potential treatment for asthma.
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Invariant NKT cells act as an adjuvant to enhance Th2 inflammatory response in an OVA-induced mouse model of asthma
Hanxiang Nie,Qiaoyu Yang,Guqin Zhang,Ailing Wang,Qing He,Min Liu,Ping Li,Jiong Yang,Yi Huang,Xuhong Ding,Hongying Yu,Suping Hu +11 more
TL;DR: The results suggest that iNKT cells may serve as an adjuvant to enhance Th2 inflammatory response in an OVA-induced murine model of asthma.
Regulatory T cells alleviate myelin loss and cognitive dysfunction by regulating neuroinflammation and microglial pyroptosis via TLR4/MyD88/NF-κB pathway in LPC-induced demyelination
Yao Wang,Dilinuer Sadike,Bo Huang,Ping Li,Qiao-qi Wu,Nanyang Jiang,Yongkang Fang,Guini Song,Li Xu,Wei Wang,Minjie Xie +10 more
TL;DR: In this article , the role of regulatory T cells (Tregs) in pyroptosis and their involvement in LPC-induced demyelination have been investigated and shown that depletion of Tregs aggravated microgliosis, inflammatory responses, immune cells infiltration and led to exacerbated myelin injury as well as cognitive defects.
A potential immunopathogenic role for reduced IL-35 expression in allergic asthma.
TL;DR: IL-35 can effectively suppress the proliferation and IL-4 production of activated CD4+CD25− T cells in allergic asthma, and that IL-35 may be a new immunotherapy for asthma patients is suggested.
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Store-operated Ca2+ entry is involved in transforming growth factor-β1 facilitated proliferation of rat airway smooth muscle cells.
TL;DR: Investigating the role and underlying mechanisms of store-operated Ca2+ entry (SOCE) in mediating the promoting effect of transforming growth factor (TGF)-β1 on the proliferation of airway smooth muscle cells (ASMCs) demonstrated that TGF-β1 promotes ASMC proliferation partly through increasing the expression and activity of SOC channels.
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