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Steven K. Lundy, Ph.D.
Regulation of the immune system in autoimmunity (particularly rheumatoid arthritis), asthma, cancer and transplantation
My research is focused on studying the interactions of B cells with T cells in animal models of arthritis and other in vivo and in vitro systems. The underlying hypothesis of all of my current work is that B cells are a regulatory cell population that can be used to control the activity of antigen-specific T cells. This hypothesis is predicated on the findings that B cells, especially the B-1a subset, express Fas ligand and can deliver death signals to antigen-specific T cells. I have published three research articles demonstrating this property of B cells, and I am currently working on a review article that will outline not only our current understanding of Fas ligand expression by B cells, but also other immunosuppressive properties of B cells. Such a review article has never been published before, despite the fact that several labs have been working in this area and finding strong evidence of the participation of B cells in the control of immune reactions. Ongoing research projects include: 1) studies of human and mouse B cell expression of Fas ligand, 2) studies on the requirements during T and B cell interactions that control T cell death and/or T cell activation, 3) regulation of B cells by Th17 cells and vice versa, 4) development of alternative models of arthritis based on reactivity to human cartilage glycoprotein 39 and citrullinated proteins in mice transgenic for human MHC DRB1*0401, and 5) collaboration with Michael Mayer in Biomedical Engineering on a study of the diagnostic potential of measuring the K+ gated channel, Kv1.3, on T and B cells in patients with multiple sclerosis, rheumatoid arthritis, and other conditions. I currently hold grants from the NIH NIAMS, the Arthritis Foundation, and the Dryer Foundation that support my work involving B cells, Fas ligand and autoreactive Th17 cells.
Tesmer LA, Lundy SK, Sarkar S, Fox DA. Th17 and human disease. Immunol Rev . 2008 Jun; 223 : 87-113. Tran CN, Lundy SK, White PT, Endres JL, Motyl CD, Gupta R, Wilke CM, Shelden EA, Chung KC, Urquhart AG, Fox DA. Molecular Interactions Between T Cells and Fibroblast-like Synoviocytes: Role of Membrane TNF a on Cytokine-Activated T Cells. Amer. J. Path., 171(5):1588-1598, 2007. Lundy SK , Sarkar S, Tesmer LA, Fox DA: Cells of the synovium in rheumatoid arthritis: T lymphocytes. Review. Arth. Res. & Ther. 9(1):202-212, 2007. Tran CN, Davis MJ, Tesmer LA, Endres JL, Motyl CD, Smuda C, Somers EC, Chung KC, Urquhart AG, Lundy SK, Kovats S, Fox DA. Presentation of arthritogenic peptide to antigen-specific T cells by fibroblast-like synoviocytes. Arth. & Rheum. 56(5):1497-1506, 2007. Lundy SK, Berlin AA, Martens TF, Lukacs NW: Deficiency of regulatory B cells increases allergic airway inflammation. Inflamm. Res. 54:514-521, 2005. Tran CN, Lundy SK, Fox DA: Synovial biology and T cells in rheumatoid arthritis. Review. Pathophysiology 12:183-189, 2005 . Lundy SK, Berlin AA, Lukacs NW: Interleukin-12 independent downmodulation of cockroach antigen-induced asthma in mice by intranasal exposure to bacterial lipopolysaccharide. Am. J. Pathology 163(5):1961-1968, 2003. Lundy SK, Boros DL: Fas ligand-expressing B-1a lymphocytes mediate CD4+ T cell apoptosis during schistosomal infection: Induction by IL-4 and IL-10. Infect. & Immun. 70(2):812-819, 2002. Lundy SK, Lerman SP, Boros DL: Soluble egg antigen (SEA)-stimulated T helper lymphocyte apoptosis and evidence for cell death mediated by FasL+ T and B cells during murine Schistosoma mansoni infection. Infect. & Immun.: 69(1):271-280, 2001.
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