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Rebecca Shilling
Section of Pulmonary / Critical Care
Assistant Professor of Medicine
e-mail:
rshillin@medicine.bsd.uchicago.edu
Referring Physician Access Line:
1-877-DOM-2730
Training:
Degree
Year
Institution
Area
BA
1991
Cornell University
Biol. Sci.
MD
1997
Case Western Reserve University
Residency
2000
Case Western Reserve University
Internal Medicine
Fellowship
2004
University of Chicago
Pulmonary and Critical Care Medicine
Academic Interests:
Dr. Shilling's research is focused on investigating the role of one of the family of co-receptors on T cells, ICOS, and its role in the Th2 responses characteristic of asthma and allergy. Specifically she is investigating the role of polymorphisms in the promoter region of ICOS and their relationship to Th2 responses in humans. In addition, she is using a mouse model of allergic airway disease to understand the role of ICOS in Th2-mediated inflammation
Representative Publications:
Shilling, R.A., J.M.Pinto, D.C. Decker, D.H. Schneider, H. Bandukwala, J. Schneider, B. Camoretti-Mercado, C. Ober, and A.I. Sperling. 2005. A Promoter Region Polymorphism in the ICOS Gene Correlates with Expression Levels on T Cells and is Associated with Atopy. J. Immunol. 175(4):2061-5.
Tong, J., D.D. Balachandran, R.A. Shilling, R.A. Anders, H.S. Bandukwala, B.S. Clay, B. Chen, Y. Qin, J.V. Weinstock, P.A. Padrid, J. Solway, K.J. Hamann, and A.I. Sperling. 2006. Fas-positive T cells regulate the resolution of airway inflammation in a murine model of asthma. J. Exp. Med. 203:1173–1184.
Shilling, R.A., H.S. Bandukwala, A.I. Sperling. 2006. Regulation of T:B cell interactions by the Inducible Costimulator molecule: Does ICOS “induce” disease? Clin. Immunol. 121(1): 13-18.
Rubin, D.T., S. Sohi, R. A. Shilling, and S. White. 2006. Pulmonary eosinophilia associated with infliximab treatment of Crohn’s disease. Gastroenterology and Hepatology. 2(8): 592-596.
Bandukwala, H.S., B.S. Clay, J. Tong, P.D. Mody, J.L. Cannon, R.A. Shilling, J.S. Verbeek, J.V. Weinstock, J. Solway, and A.I. Sperling. 2006. Signaling through FcγRIII is required for optimal Th2 responses and Th2-mediated airway inflammation. J Exp Med. 204(8):1875-89.