Investigator, The Feinstein Institute for Medical Research
Professor of Molecular Medicine, Hofstra North Shore-LIJ School of Medicine
Phone: (516) 562-3840
Anne Davidson, MBBS, is professor of Molecular Medicine at Hofstra North Shore-LIJ School of Medicine and investigator at the Feinstein Institute for Medical Research. She received her MBBS degree from the University of Melbourne, Australia and is a board certified Rheumatologist. She is currently the program director of the Rheumatology fellowship at the North Shore-LIJ Health System. Dr. Davidson is a member of the medical advisory board for the NY SLE Foundation and co-chairs the grant review committee of the animal models subsection for the Lupus Research Institute. She is currently the chair of the scientific advisory council for the Rheumatology Research Foundation.
The current interests of Dr. Davidson’s laboratory are focused on pathogenesis and therapy of SLE, an autoimmune disease affecting women of childbearing years. Production of autoantibodies directed against ubiquitous cellular components, such as DNA and other nuclear antigens, results in formation of immune complexes that can deposit in target tissues and initiate inflammation that causes organ damage. Other immune cells also become activated and contribute to the inflammatory process.
The first goal of the laboratory is to understand more about the regulation of autoantibody producing B cells and to use newly-discovered pathways of immune activation to design and test novel therapies for SLE. New therapies for SLE have become possible with the discovery that the activation of T cells requires two signals. The first signal is based on recognition of a specific antigen. The second signal is based on a conserved set of molecules on the surface of T cells called co-stimulatory receptors. When these are engaged by the appropriate co-stimulatory ligand in the presence of signal 1, cell activation proceeds. B cells also receive co-stimulatory or survival signals that synergize with signals received through the B cell receptor. Drugs based on modulating the effects of co-stimulation can therefore prevent or alter activation of both T and B cells. Several co-stimulatory agents are being used in the laboratory in three different mouse models of SLE, including one model of proliferative nephritis, one model of sclerosing kidney disease and a model of anti-phospholipid syndrome. Mice with knock-in of anti-DNA and anti-cardiolipin heavy chains have been bred into these models to allow study of the effects of treatment on B cell selection.
The second goal of the laboratory is to understand the role of co-stimulatory molecules in target organ inflammation. Co-stimulatory receptors are involved in trafficking of immune cells to target organs. Normally, immune cells are sequestered in the lymphoid organs, such as the spleen and lymph nodes. When they traffic to a non-lymphoid organ, such as the kidney, they can induce inflammation. Recent work therefore focuses on lupus nephritis and the role of immune cell activation in kidney damage so as to understand the molecular basis for cell migration to the kidney and for resolution of inflammation after remission inducing therapies.
In collaboration with Nephrologists at Mount Sinai and University of Michigan, the laboratory has constructed a molecular profile of renal inflammation and remission that has generated several testable hypotheses. Further studies will address whether similar profiles are found in human SLE.
Finally, translational studies are being performed in the setting of clinical trials to determine the efficacy and mechanism of action of new biologic agents that target immune activation in humans.
Ramalingam Bethunaickan, PhD
Postdoctoral Research Fellow
Education: PhD in Biomedical Science 2003 from Tuberculosis Research Center (ICMR), and MGR Medical University, Chennai, India
Research: Mechanism of Remission of Lupus Nephritis. Stage-Specific Molecular profiling for Lupus Nephritis among different murine models of SLE. Understanding pathogenesis of SLE nephritis, improved therapeutic strategies and identification of potential biomarkers within these models. Studies remission mechanisms in lupus nephritis, and works on renal inflammation in lupus.
Phone: (347) 803-3644
Weiqing Huang, MD
Education: MD; Beijing Medical University, Beijing China
Research: My research work focuses on the pathogenesis of SLE, and the mechanism of action of novel co-stimulatory molecules on the immune system both in murine models and patients with SLE.
Phone: (646) 418-9126
Zheng (Steve) Liu
Phone: (646) 421-5145
Phone: (718) 810-1509
Post Doc Research Fellow
Phone: (347) 331-7073
Phone: (678) 643-6659
Phone: (516) 445-3031
Phone: (646) 305-8831
Phone: (347) 599-6584
University of Melbourne, Australia
Field of Study: Medicine
1983 D.E.V. Starr Overseas Travelling Fellowship in Rheumatology Awarded by Royal Australian College of Physicians
1985 1988 Fellow Damon Runyon Walter Winchell Cancer Fund
1985 Fellow Royal Australasian College of Physicians (FRACP)
1986 ARA (ACR) Senior Fellow Award
1988-1993 NIH Clinical Investigator Award
1990-2000 Board certified Internal Medicine
1992-2012 Board certified Rheumatology
2006-2009 Kirkland Scholar Award
2009 Recipient Dubois Award American College of Rheumatology Annual Meeting
- Sahu R, Bethunaickan R, Edegbe O and A Davidson. “Structure and function of renal macrophages and dendritic cells from SLE-prone mice.” Arthritis Rheum 66:1596-1607 2014
Supplementary Data Sheet
- Jacobi AM, Huang W, Wang T, Freimuth W, Sanz I, Furie R, Mackay M, Aranow C, Diamond B and A Davidson. “The Effect of Prolonged Treatment with Belimumab on B cells in Human SLE.” Arthritis and Rheumatism 62(1):201-210 2010. PMC2857977
- Triantafyllopoulou A, Franzke C-W, Seshan S V, Perino G,. Kalliolias G D, Ramanujam M, van Rooijen N, Davidson A, and L B Ivashkiv. “Proliferative lesions and metalloproteinase activity in murine lupus nephritis mediated by type I interferons and macrophages.” Proc. Natl. Acad. Sci. 107(7):3012-7 2010.
- Ramanujam M, Bethunaickan R, Huang W, Tao H, Madaio MP and A Davidson. “Selective blockade of BAFF prevents and treats SLE nephritis in NZM2410 mice.” Arthritis and Rheumatism 62(5):1457-68 2010. PMC2917190
- Liu Z, Bethunaickan R, Huang W, Lodhi U, Solano I, Madaio MP, and A Davidson. “Interferon alpha Accelerates Murine SLE in a T Cell Dependent Manner.” Arthritis and Rheumatism 63:219-29 2011. PMC3014995
Supplementary Data Sheet
- Bethunaickan R, Berthier C, Ramanujam M, Zhang W, Bottinger E, Kretzler M and A Davidson. “A unique hybrid renal mononuclear phagocyte activation phenotype in murine SLE nephritis.” J. Immunol. 186:4994-5003 2011. PMC3159403
- Liu Z, Bethunaickan R, Huang W, Ramanujam, M, Madaio MP, and A Davidson. “IFN confers resistance of SLE nephritis to therapy in NZB/W F1 mice.” J. Immunol. 187(3):1506-13 2011. PMC3140572
- Huang W, Moisini I, Bethunaickan R, Sahu R, Akerman M, Eilat D, Lesser M, and A Davidson. “BAFF inhibition decreases selection of naïve but not antigen induced autoreactive B cells in murine SLE.” J. Immunol. 187(12):6571-80 2011. PMC3263361
- Berthier CC, Bethunaickan R, Gonzalez-Rivera T, Nair V, Ramanujam M, Zhang W, Bottinger EP, Segerer S, Davidson A* and M Kretzler* (co-corresponding authors). “Cross-species transcriptional network analysis defines shared inflammatory responses in murine and human lupus nephritis J.” Immunol 2012 Jul 15;189(2):988-1001. PMC3392438
- Bethunaickan R, Sahu R, Liu Z, Tang Y, Huang W, Ramanujam M, Madaio MP, and A Davidson. “TNF alpha prevents treats SLE nephritis by preventing the macrophage effector response to glomerular immune complexes.” Arthritis Rheum. 2012 Oct;64(10):3399-408. PMC3443508
- Moisini I, Huang W, Bethunaickan R, Sahu R, Akerman M, Marion T, Lesser M, and A Davidson. “The Yaa locus and IFN fine tune germinal center B cell selection in murine SLE. J Immunol.” 2012 Nov 1;189(9):4305-12