The Administrative Core will be the central office of the Philadelphia ACE. Dr. A.M. Rostami will be the director of this core. The Administrative Core will be responsible for all the administrative functions related to the research projects. It will provide a centralized office for all the research groups. The principal responsibilities of the Administrative Core will be: 1) budget management;2) administrative functions (e.g. regulatory and compliance issues, progress reports);3) communication with outside institutions/offices (e.g., ACE representation);4) coordination of activities between different segments of multi-project programs (e.g., coordination between Pis and co-Pis regarding monthly and quarterly meetings, producing and distributing supporting material);5) organizational, collaborative and public relations activities (e.g., organizing annual retreat and seminar series, informing the wider scientific community about activities of the ACE, launching and maintaining a website dedicated to the Philadelphia ACE, its activities and progress).
The Administrative Core will facilitate activities of the Philadelphia ACE through budget management, coordination, administrative and secretarial support, public relations, etc. These Core activities are essential to efficient functioning of the ACE. Thus, relevance of the Administrative Core lies in helping ACE to fulfill its goals.
|Xie, Chong; Ciric, Bogoljub; Yu, Shuo et al. (2016) IL-12R?2 has a protective role in relapsing-remitting experimental autoimmune encephalomyelitis. J Neuroimmunol 291:59-69|
|Rasouli, Javad; Ciric, Bogoljub; Imitola, Jaime et al. (2015) Expression of GM-CSF in T Cells Is Increased in Multiple Sclerosis and Suppressed by IFN-? Therapy. J Immunol 194:5085-93|
|Lee, Iris J; Hilliard, Brendan A; Ulas, Mehriban et al. (2015) Monocyte and plasma expression of TAM ligand and receptor in renal failure: Links to unregulated immunity and chronic inflammation. Clin Immunol 158:231-41|
|Shao, Wen-Hai; Zhen, Yuxuan; Finkelman, Fred D et al. (2014) The Mertk receptor tyrosine kinase promotes T-B interaction stimulated by IgD B-cell receptor cross-linking. J Autoimmun 53:78-84|
|Fitzgerald, Denise C; Fonseca-Kelly, Zoë; Cullimore, Melissa L et al. (2013) Independent and interdependent immunoregulatory effects of IL-27, IFN-?, and IL-10 in the suppression of human Th17 cells and murine experimental autoimmune encephalomyelitis. J Immunol 190:3225-34|
|Zizzo, Gaetano; Guerrieri, Justus; Dittman, Lindsay M et al. (2013) Circulating levels of soluble MER in lupus reflect M2c activation of monocytes/macrophages, autoantibody specificities and disease activity. Arthritis Res Ther 15:R212|
|Zizzo, Gaetano; Cohen, Philip L (2013) IL-17 stimulates differentiation of human anti-inflammatory macrophages and phagocytosis of apoptotic neutrophils in response to IL-10 and glucocorticoids. J Immunol 190:5237-46|
|Zizzo, Gaetano; Hilliard, Brendan A; Monestier, Marc et al. (2012) Efficient clearance of early apoptotic cells by human macrophages requires M2c polarization and MerTK induction. J Immunol 189:3508-20|
|Chen, David R; Cohen, Philip L (2012) Living life without B cells: is repeated B-cell depletion a safe and effective long-term treatment plan for rheumatoid arthritis? Int J Clin Rheumtol 7:159-166|
|Singh, Namrata; Cohen, Philip L (2012) The T cell in Sjogren's syndrome: force majeure, not spectateur. J Autoimmun 39:229-33|
Showing the most recent 10 out of 18 publications