Immunology
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Shannon J. Turley

Associate Program Head, Graduate Program in Immunology

Department of Pathology
Harvard Medical School
Dept. of Cancer Immunology and AIDS
Dana Farber Cancer Institute
Dana Building, Room 1440
44 Binney Street
Boston, MA 02115

Tel: 617-632-4990
Fax: 617-582-7999
Email: shannon_turley@dfci.harvard.edu
website:The Turley Lab Page
4 Postdoctoral Fellows, 1 Graduate Student

 Shannon Turley

Adaptive immune responses begin with the stimulation of naïve T cells and subsequent generation of effector cells. T cells do not respond to antigens in their native states but rather respond to antigenic peptide bound to MHC molecules. Because circulating naïve T cells cannot usually access peripheral non-lymphoid tissues, the tissue-derived antigens they recognize must be transported to T cell zones of nearby lymphoid organs by antigen presenting cells and presented therein as surface bound peptide-MHC complexes. Dendritic cells, the most stimulatory of all antigen presenting cells, are essential players at every step of this process. Upon sufficient stimulation by a dendritic cell, antigen-specific T cells will proliferate and differentiate into both effector and memory cells, which circulate through non-lymphoid tissues and are retained where they re-recognize cognate antigen. At these sites, effector T cells will carry out their protective duties by killing infected or malignant cells.

Our lab is interested in understanding the molecular and cellular basis of T cell priming by dendritic cells in diseases such as pancreatic cancer and autoimmune diabetes. How the immunostimulatory and migratory functions of dendritic cells are influenced by unique tissue microenvironments, such as the malignant pancreas and the small intestine, is a major focus of our research. Combining mouse models of human disease with cell biological and genetic approaches and high-resolution imaging, we explore the endocytosis, processing, and delivery of tissue-restricted antigens by different dendritic cell subsets. Studies are also underway to investigate dendritic cell physiology in human cancers, specifically pancreatic adenocarcinomas and endocrine tumors. Ultimately, elucidating the steps leading to robust immune responses against self-antigens should provide the necessary framework for enhancing this process in cancer and dampening it in autoimmune diseases.

 

Papers & Publications:

1. Anderson MS, Venanzi ES, Klein L, Chen Z, Berzins S, Turley SJ, von Boehmer H, Bronson R, Dierich A, Benoist C, Mathis D. 2002. Projection of an immunological self-shadow within the thymus by the aire protein. Science 298:1395.

2. Turley S, Poirot L, Hattori M, Benoist C, Mathis D. 2003. Physiological b-cell death triggers priming of self-reactive T cells by dendritic cells in a type-1 diabetes model. J Exp Med. 198:1527-37.

3. Lee LF, Xu B, Michie S, Turley S, McDevitt HO. 2005. The role of TNFa in the pathogenesis of type-1 diabetes in the NOD mouse: Analysis of dendritic cell maturation. PNAS 102:15995-16000.

4. Turley SJ, Lee JW, Dutton-Swain N, Mathis D. Benoist C. 2005. Endocrine self and gut non-self intersect in pancreatic lymph nodes. PNAS 102: 17729-17733.

5. Lee JW, Epardaud M, Sun J, Becker JE, Cheng AC, Yonekura A, Heath JK, and Turley SJ. 2007. Peripheral antigen display by lymph node stroma promotes T cell tolerance to intestinal self. Nat. Immunol., 8:181-190.