S
Shadi Swaidani
Researcher at Cleveland Clinic
Publications - 35
Citations - 2564
Shadi Swaidani is an academic researcher from Cleveland Clinic. The author has contributed to research in topics: Inflammation & Immune system. The author has an hindex of 21, co-authored 28 publications receiving 2203 citations. Previous affiliations of Shadi Swaidani include Case Western Reserve University & Cleveland Clinic Lerner Research Institute.
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Journal ArticleDOI
The adaptor Act1 is required for interleukin 17–dependent signaling associated with autoimmune and inflammatory disease
Youcun Qian,Caini Liu,Justin Hartupee,Cengiz Z. Altuntas,Muhammet F. Gulen,Daniel Jane-wit,Jianhua Xiao,Yi Lu,Natalia Giltiay,Jinbo Liu,Tomasz Kordula,Qi-Wei Zhang,Bruce A. Vallance,Shadi Swaidani,Mark A. Aronica,Vincent K. Tuohy,Thomas A. Hamilton,Xiaoxia Li +17 more
TL;DR: The data show that Act1 is essential in IL-17-dependent signaling in autoimmune and inflammatory disease and was associated with much less inflammatory disease in vivo in both autoimmune encephalomyelitis and dextran sodium sulfate–induced colitis.
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Direct and Differential Suppression of Myeloid-Derived Suppressor Cell Subsets by Sunitinib Is Compartmentally Constrained
Jennifer S. Ko,Patricia Rayman,Joanna Ireland,Shadi Swaidani,Geqiang Li,Kevin D. Bunting,Brian I. Rini,James H. Finke,Peter A. Cohen +8 more
TL;DR: It is concluded that compartment-dependent GM-CSF exposure in resistant tumors may account for the regionalized effect of sunitinib upon host MDSC modulation and hypothesize that ancillary strategies to decrease such regionalized escape will enhance the potency of sun itinib as an immunomodulator and a cancer therapy.
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Act1, a U-box E3 Ubiquitin Ligase for IL-17 Signaling
Caini Liu,Wen Qian,Youcun Qian,Natalia Giltiay,Yi Lu,Shadi Swaidani,Saurav Misra,Li Deng,Zhijian J. Chen,Xiaoxia Li +9 more
TL;DR: It is proposed that Act1 mediates IL- 17–induced signaling pathways through its E3 ubiquitin ligase activity and that TRAF6 is a critical substrate of Act1, which indicates the importance of protein ubiquitination in the IL-17–dependent inflammatory response.
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Nitrotyrosine Proteome Survey in Asthma Identifies Oxidative Mechanism of Catalase Inactivation
Sudakshina Ghosh,Allison J. Janocha,Mark A. Aronica,Shadi Swaidani,Suzy A.A. Comhair,Weiling Xu,Lemin Zheng,Suma Kaveti,Michael Kinter,Stanley L. Hazen,Serpil C. Erzurum +10 more
TL;DR: Analysis of catalase isolated from asthmatic airway epithelial cells revealed increased amounts of several protein oxidation markers, including chloro- and nitrotyrosine, linking oxidative modification to the reduced activity in vivo.
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The inducible kinase IKKi is required for IL-17-dependent signaling associated with neutrophilia and pulmonary inflammation
Katarzyna Bulek,Caini Liu,Shadi Swaidani,Liwen Wang,Richard C. Page,Muhammet F. Gulen,Tomasz Herjan,Amina Abbadi,Wen Qian,Dongxu Sun,Mark E. Lauer,Vincent C. Hascall,Saurav Misra,Mark R. Chance,Mark A. Aronica,Thomas A. Hamilton,Xiaoxia Li +16 more
TL;DR: IKKi is a kinase newly identified as modulating IL-17 signaling through its effect on Act1 phosphorylation and consequent function, and is found that IKKi was required forIL-17-induced expression of genes encoding inflammatory molecules in primary airway epithelial cells, neutrophilia and pulmonary inflammation.