Steven K. Lundy, Ph.D.
Regulation of the immune system in autoimmunity, asthma, cancer and infections by B lymphocytes
Our laboratory studies immune regulation of T lymphocytes at the level of interactions with antigen presenting cells. Over stimulation and/or deficient suppression of T cells is a major problem in autoimmune diseases and allergy. In contrast, poor stimulation or over-suppression of T cells can lead to decreased immune responses to infectious agents and/or inadequate tumor surveillance. The broad goal is to better understand the interactions between T cells and APC that cause disease, and to design methods to manipulate these interactions as treatment strategies. The current emphasis is on understanding the biology and effector functions of Fas ligand-positive, ‘killer’ B lymphocytes in animal models of autoimmune arthritis. Other projects include: 1) characterizing Fas ligand expression in human B cells; 2) identifying killer B cell subsets in mice; 3) developing new models of arthritis in mice; 4) studying T cell interactions with patient-derived synovial fibroblasts that act as antigen presenting cells; and 5) using natural exosomes and plastic beads to modulate T cell reactions in vitro and in vivo. Our lab has active collaborations with many Immunology Program faculty, as well as collaborations with the Dental School, School of Public Health, the Biomedical Engineering Department, and the Kellogg Eye Center.
We currently have funding from an NIH-NIAID R03 grant and are part of the UM Autoimmune Center of Excellence, which will also be funded by the NIH-NIAID.
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. PMCID 11796615
Lundy SK, Berlin AA, Martens TF, Lukacs NW: Deficiency of regulatory B cells increases allergic airway inflammation. Inflamm. Res. 54:514-521, 2005. 16389573
Tesmer LA, Lundy SK, Sarkar S, Fox DA. Th17 and human disease. Review. Immunological Reviews, 223:87-113, 2008. PMCID 18613831
Lundy SK. Killer B lymphocytes: The evidence and the potential. Review. Inflammation Research, 58(7):345-357, 2009. PMCID 19262989
Lundy SK, Fox DA. Reduced Fas ligand-expressing splenic CD5+ B lymphocytes in severe collagen-induced arthritis. Arthritis Res. Ther., 11(4):R128 EPub ahead of print, 2009. PMCID 19706160
Klinker MW, Lundy SK. Multiple mechanisms of immune suppression by B lymphocytes. Review. Molecular Medicine, 18(1):123-137, 2012. PMCID 3276396
Marchesan JT, Morelli T, Lundy SK, Jiao Y, Lim S, Inohara N, Nunez G, Fox DA, Giannobile WV. Divergence of the systemic immune response following oral infection with distinct strains of Porphyromonas gingivalis. Mol. Oral Microbiol., 27(6):483-495, 2012. PMID 23134613
Lundy SK, Lukacs NW. Chronic schistosome infection leads to modulation of granuloma formation and systemic immune suppression. Front. Immunol., 4:39. doi:10.3389/fimmu.2013.00039. Epub 2013 Feb 20. PMCID 3576626
Szymczak WA, Davis MJ, Lundy SK, Dufaud C, Olszewski M, Pirofski LA. mBio 2013 Jul 2;4(4). doi:pii: e00265-13. 10.1128/mBio.00265-13. PMID 23820392
Klinker MW, Reed TJ, Fox DA, Lundy SK. Interleukin-5 supports the expansion of Fas ligand-expressing killer B cells that induce antigen-specific apoptosis of CD4+ T cells and secrete interleukin-10. PLOS One 2013 Aug. 5; 8(8):e70131.doi 10.1371/journal.pone.0070131. PMID23940537, PMC3734024
Marchesan JT, Gerow EA, Schaff R, Taut AD, Shin SY, Sugai J, Brand D, Burberry A, Jorns J, Lundy SK, Nunez G, Fox DA, Giannobile WV. Porphyromonas gingivalis exacerbates the severity of collagen-induced arthritis via Th17 cell responses. Arth Res Ther, 2013 Nov. 12, 15(6):R186. doi: 10.1186/ar4376. PMID24456966, PMC3979094