Department of Medicine Faculty Profile

Anne Sperling
Section of Pulmonary / Critical Care
Associate Professor of Medicine
Faculty Director, Immunological Applications Core Facility; Member, Committee in Immunology
e-mail: asperlin@medicine.bsd.uchicago.edu

Training:

Degree	Year	Institution	Area
AB	1984	Smith College	Biology
PhD	1990	Tufts University	Immunology
Fellowship	1994	The University of Chicago	Committee on Immunology

Academic Interests:

Dr. Sperling’s laboratory is investigating the role of co-receptors in T cell function. Understanding these key regulators of T cell responses is essential for determining mechanisms involved in the development of asthma and other lung diseases. Areas of emphasis include 1) ICOS regulation of Th2 inflammation in asthma models; 2) genetic variation of the ICOS gene in human allergy; 3) CD43 regulation of T cell activation; 4) Fas regulation of clearance of Th2 mediated inflammation.

Representative Publications:

Tong J., E.J. Allenspach, S. Takahashi, P.D. Mody, C. Park, J.K. Burkhardt, A.I. Sperling. 2004. CD43 regulation of T cell activation is not through steric inhibition of T cell-APC interactions but through an intracellular mechanism. J.Exp. Med. 199:1277-1283.
Allenspach, E.J., Cullinan, P., Q. Tang, J. Tong, S.M. Takahashi, R. Morgan, J.K. Burkhardt, and A. I. Sperling. 2001. ERM-dependent movement of CD43 defines a novel protein complex distal to the immunological synapse. Immunity. 15:739.
Tesciuba, A.G., S. Subudhi, R. Rother, S.J. Faas, A. Frantz, D.E. Elliot, J. Weinstock, L.A. Matis, J.A. Bluestone, and A.I. Sperling. 2001. Inducible costimulator molecule (ICOS) regulates Th2 effector function but not Th2 differentiation in vivo. J. Immunol. 167:1996.
Douglas, I.S., A.R. Leff, and A.I. Sperling. 2000. Specific adherence of T cell and eosinophils mediated by ICAM-3 results in eosinophil activation. J. Immunol. 164:3385.
Sperling, A.I., J.R. Sedy, N. Manjunath, A. Kupfer, B. Ardman and J.K. Burkhardt. 1998. Cutting Edge: T cell receptor signaling induces selective exclusion of CD43 from the T-APC contact site. J. Immunol. 161:6459.