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  • Professor, Center for Autoimmune, Musculoskeletal and Hematopoietic Diseases, Feinstein Institutes for Medical Research
  • Professor of Molecular Medicine, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell

About the investigator

Anne Davidson, MBBS, is professor of Molecular Medicine at the Donald and Barbara Zucker School of Medicine at Hofstra/Northwell and investigator at the Feinstein Institutes 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 Northwell Health. 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.

Research focus

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.

Lab members

Weiqing Huang, MD
Research Associate
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.
E-mail: [email protected]
Phone: (646) 418-9126

Zheng (Steve) Liu
Graduate Student
E-mail: [email protected]
Phone: (646) 421-5145

Peta-Gay Ricketts
Research Assistant
Phone: (718) 810-1509

George Scott
Research Assistant
Phone: (678) 643-6659

Ingrid Solano
Research Assistant
E-mail: [email protected]
Phone: (516) 445-3031

Haiou Tao
Research Assistant
E-mail: [email protected]
Phone: (646) 305-8831

Shitij Aurora
Elmezzi Student
Phone: (347) 599-6584

Education

University of Melbourne, Australia
Degree: MBBS
1978
Field of study: Medicine

Honors & awards

  • 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

Publications

  1. 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
  2. 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
  3. 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.
  4. 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 Rheumatism62(5):1457-68 2010. PMC2917190
  5. 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
  1. 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
  2. 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
  3. 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
  4. 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
  5. 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
  6. 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
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