| This NIH funded laboratory investigates the molecular and cellular determinants of alloantigen specific tolerance using murine models of cardiac and pancreatic islet transplantation. Specific investigations involve the determination of mechanisms responsible for remodeling of secondary lymphoid organ structure, and how those mechanisms drive T cell migration, differentiation, and fate determination. The molecular focus of the investigations is directed to chemokines, chemokine receptors, cytokines, sphingosine receptors, lymphotoxin, and stromal fibers. Specific cellular elements include regulatory suppressive T cells, effector T cells, vascular and lymphatic endothelial cells, stromal cells, and dendritic cell subsets. Techniques include heavy reliance on in vivo animal models, migration and trafficking assays, real time imaging and advanced microscopy, multicolor flow and sorting, and a variety of molecular techniques for proteins and nucleic acids.|
Warren KJ, Iwami D, Harris DG, Bromberg JS, Burrell BE. Vascular basement membrane proteins laminin alpha 4 and laminin alpha 5 differentially influence CD4+ T cell lymph node trafficking and allograft fate. J. Clin. Invest. 2014; 124:2204-2218.
Xiong Y, Ahmad S, Iwami D, Brinkman CC, Bromberg JS. T-bet regulates natural Treg afferent lymphatic migration and suppressive function. J. Immunol. 2016; 196:2526-2540.
Brinkman CC, Iwami D, Hritzko MK, Xiong, Y Ahmad, Bromberg JS. Treg engage lymphotoxin beta receptor for afferent lymphatic transendothelial migration. Nature Communications 2016; in press.
Please send letter of interest, your contact information, CV, and list of three references to:
Jonathan S. Bromberg, MD, PhD
Professor of Microbiology and Immunology
Center for Vascular and Inflammatory Disease
University of Maryland
29 S. Greene St., Suite 200
Baltimore, MD 21201