Theresa T. Lu, MD, PhD

Selected Publications

Lu TT, Cyster JG.  Integrin-mediated long-term B cell retention in the splenic marginal zone.  Science.  2002;297: 409-412.

Cyster JG, Ansel KM, Ngo VN, Hargreaves, Lu TT.  Traffic patterns of B cells and plasma cells.  Advances in Experimental Medicine and Biology.  2002;512: 35-41.

Lo CG, Lu TT, Cyster JG.  Integrin dependence of lymphocyte entry into the splenic white pulp.  Journal of Experimental Medicine. 2003;197: 353-61.

von Scheven E, Lu TT, Emery H, Elder M, Wara D.  Thrombosis and pediatric Wegener’s granulomatosis:  acquired and genetic risk factors for hypercoaguability.  Arthritis and Rheumatism. 2003;49: 862-5.

Lu TT.  Up and coming therapeutics:  FTY720. Pediatric Rheumatology Online J.  2004;2: 359-365.

Kabashima K, Banks TA, Ansel KM, Lu TT, Ware CF, Cyster JG.  Intrinsic lymphotoxin-beta receptor requirement for homeostasis of lymphoid tissue dendritic cells.  Immunity. 2005;22: 439-450.

Hu X, Paik PK, Chen J, Yarlina A, Kockeritz L, Lu TT, Woodgett, JR, Ivashkiv LB.  IFN-gamma suppresses IL-10 production and synergizes with TLR2 by regulating GSK3 and CREB/AP-1 Proteins.  Immunity. 2006; 24: 563-674.

Webster B, Ekland EH, Agle LM, Chyou S, Ruggieri R, Lu TT.  Regulation of lymph node vascular growth by dendritic cells.  Journal of Experimental Medicine.  2006; 203: 1903-1913. (Cover and highlighted article).

Chyou S, Ekland EH, Carpenter AC, Tzeng T, Tian S, Michaud M, Madri JA, and Lu TT.  Fibroblast-type reticular stromal cells regulate the lymph node vasculature. Journal of Immunology.  2008;  181:3887-3896.

Gordon JK, Magro C, Lu T, Schneider R, Chiu A, Furman RR, Solomon G, Bass A, Erkan D.  Overlap between systemic lupus erythematosus and Kikuchi Fujimoto disease:  a clinical pathology conference held by the Department of Rheumatology at Hospital for Special Surgery.  HSS Journal.  2009; 2:169-177.

Tzeng T, Chyou S, Tian S, Webster B, Carpenter AC, Guaiquil VH, and Lu TT.  CD11chi dendritic cells regulate the  reestablishment of vascular quiescence and stabilization after immune stimulation of lymph nodes.   Journal of Immunology.  2010; 184:4247-4257.

Penack O, Henk E, Suh D, King CG, Smith OM, Na IK, Holland AM, Ghosh A, Lu SX, Jenq RR, Liu C, Murphy GF, Lu TT, May C, Scheinberg DA, Gao DC, Mittal V, Benezra R, van den Brink MR.  Depletion of Vascular Endothelial Progenitor Cells Inhibits Inflammation.  Journal of the National Cancer Institute.  2010. 12:894-908.

Chyou S, Benahmed F, and Lu TT. Coordinated regulation of lymph node vascular-stromal growth first by CD11c+ cells and then by T and/or B cells.  Journal of Immunology. In Press.

Lu TT. Invited review “Dendritic cells: Novel players in fibrosis and scleroderma.”  Current Rheumatology Reports.  In Press.

Lu TT, Kim H, Ma X. IL-17 a new kid on the block of tertiary lympoid organs. Cell Mol Immunol. 2011 Sep 19. doi: 10.1038/cmi.2011.34

For more publications, please see the PubMed listing.

Research Description

Lymphoid Tissue Vascular-Stromal Regulation and Function

Secondary lymphoid tissues such as lymph nodes are the sites of primary immune responses. These lymphoid tissues grow rapidly and robustly during an immune response, and this growth is accompanied by growth of the blood vessels. Although work in recent years has delineated the regulation of vascular growth in a number of systems, the regulation of lymphoid tissue vessel growth is not well understood. However, because blood vessels of the lymphoid tissues are critical for the delivery of oxygen, micronutrients, and cells, manipulating the growth of blood vessels may be a means to manipulate immune function.

We have identified a role for dendritic or other CD11c+ cells and for fibroblastic reticular cells in regulating lymph node vascular growth. In lymph nodes, blood vessels are suspended in a reticular network composed of collagen-rich fibrils that are ensheathed by fibroblastic reticular cells. We have shown that fibroblastic reticular cells are the main VEGF mRNA-expressing cell type within lymph nodes. Dendritic cells are directly attached to the reticular network and are enriched in vessel-rich areas. Our model is currently that dendritic cells that are activated by the immune stimulus induce fibroblastic reticular cells to upregulate VEGF, which leads to endothelial cell proliferation. Dendritic cells are best known for their function in presenting antigen to T cells; we propose that also play a role in preparing the lymph node vascular-stromal microenvironment for the ensuing immune response.

After vascular expansion, there is a stage of vascular quiescence and stabilization whereby proliferation of the newly expanded vasculature is downregulated and the vessels are made less leaky. We have identified a role for a distinct subset of late-accumulating dendritic cells in regulating vascular quiescence and stabilization and are currently trying to understand how these dendritic cells work. We have also shown that disruption of vascular quiescence and stabilization is associated with disrupted B cell responses. Abnormal B cell responses in autoimmune diseases such as lupus lead to the generation of pathogenic autoantibodies which cause inflammation in skin, kidney and other internal organs. We are testing the possibility that disruption of vascular quiescence and stabilization could be a novel means by which to control pathogenic autoantibody generation.

Interested postdoc applicants should send cover letter, CV, and contacts for 3 references to lut@hss.edu

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Contact Information

Office Locations

Caspary Research Building
541 East 71st Street
New York, NY 10021

Tel:  212.774.2532

Mailing Address

Hospital for Special Surgery
535 East 70th Street
New York, New York 10021