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Julie Lang, PhD

Senior Research Associate, Assistant Director Humanized Mouse Core HI³

Julie Lang, PhD
​12800 E. 19th Avenue, Mail Stop 8333
RC1N P18-840-D
Aurora, Colorado 800451
​1996 ​PhD ​Immunology and Microbiology | University of Colorado Health Sciences Center | Denver, CO
​1987 BS
​Chemical Engineering | Georgia Institute of Technology | Atlanta, GA
​1985-86 ​Scholarship | Eidgenossiche Technische Hochschule | Zurich, SZ
​1985-86 ​YMCA Swiss-American Exchange Scholarship
​1988 ​Outstanding Technical Award, IBM
​1990-91 ​Colorado Commission on Higher Education Doctoral Fellowship, University of Colorado Health Sciences Center
​1991-96 ​Howard Hughes Pre-doctoral Fellowship
​1998 ​Blum Kovlar Barbara Davis Center for Childhood Diabetes Postdoctoral Fellowship
​1998-00 ​Juvenile Diabetes Foundation Postdoctoral Fellowship
​2006-07 ​Arthritis National Research Foundation Scholar
​Dr. Julie Lang graduated from the Georgia Institute of Technology with a B.S. in Chemical Engineering in 1987. After working as a semiconductor engineer for IBM in Manassas, VA she enrolled in graduate school at the University of Colorado Health Sciences Center and earned her Ph.D. in Microbiology and Immunology in 1996. She has remained in Colorado, first as a postdoctoral fellow under the supervision of Dr. Donald Bellgrau from 1998-2004, and then as an Instructor in the Department of Rheumatology working with Dr. Susan Boackle from 2004-2007. In addition to her research, Dr. Lang taught general biology courses at the undergraduate level at Metropolitan State College. In 2008, she began a humanized mouse project with Dr. Roberta Pelanda at National Jewish Health. With Dr. Pelanda’s move to the University of Colorado Denver AMC in 2014, Drs. Lang and Pelanda brought their expertise and humanized mouse model to this campus. This work established the foundation for the humanized mouse core within the Human Immunology and Immunotherapy Initiative (HI3).
​Dr. Lang’s research focuses on understanding basic mechanisms of B cell development and tolerance with the goal of defining deficits in these processes that may contribute to autoimmunity.  Her graduate thesis, under the mentorship of Dr. David Nemazee, investigated mechanisms of both central and peripheral B cell tolerance in an immunoglobulin transgenic mouse model.  She then went on to study mechanisms of autoimmunity in type 1 diabetes with Dr. Donald Bellgrau with a focus on the role of TCR signaling strength in T cell tolerance.  Her work with Dr. Susan Boackle continued in the field of B cell tolerance with studies on the contribution of polymorphisms of CD21, a co-receptor for B cell receptor signaling, in systemic lupus erythematosus and rheumatoid arthritis.  Working together with Dr. Roberta Pelanda, her research has extended to studying mechanisms of immunological tolerance and selection in human B cells. They use hematopoietic humanized mice, generated by transplanting human hematopoietic stem cells from umbilical cord blood into immunodeficient mice, to determine how human B cells develop and undergo selection.  Using a unique humanized mouse model in which one can follow the fate of specific B cells as they develop, Drs. Pelanda and Lang have shown that receptor editing and tolerance occur in immature human B cells similar to mouse B cells although there is a range of responses observed among B cells with different genetics. They are currently using this model to help understand processes that interfere with B cell selection and predispose individuals to autoimmunity.
  • ​O’Brien, R.L., M.P. Happ, A. Dallas, R. Cranfill, L. Hall, J. Lang, Y.X. Fu, R. Kubo, and W. Born. 1991. Recognition of a single hsp-60 epitope by an entire subset of gamma delta T lymph ocytes. Immun. Rev. 121: 155-70.
  • O’Brien, R.L., Y.X. Fu, R. Cranfill, A. Dallas, C. Ellis, C. Reardon, J. Lang, S.R. Carding, R. Kubo, and W. Born. 1992. Heat shock protein Hsp60-reactive gamma delta cells: a large, diversified T-lymphocyte subset with highly focused specificity. Proc. Natl. Acad. Sci. of USA. 89: 4348-52.
  • Lang, J., M. Jackson, L. Teyton, A. Brunmark, K. Kane, and D. Nemazee.  1996. B cells are exquisitely sensitive to clonal elimination induced by ultralow affinity, membrane-bound antigen. J. Exp. Med. 184:1685-1697.
  • Lang, J., B. Arnold, G. Hammerling, A. W. Harris, S. Korsmeyer, D. Russell, A. Strasser, and D. Nemazee. 1997. Enforced Bcl-2 expression inhibits antigen-mediated clonal elimination of peripheral B cells in an antigen dose-dependent manner, and promotes receptor editing in autoreactive, immature B cells.  J. Exp. Med.  186:1513-1522.
  • Nemazee, D., V. Kouskoff, M. Hertz, J. Lang, D. Melamed, K. Pape and M. Retter. 2000.  B-cell-receptor-dependent positive and negative selection in immature B cells.  Curr Top Microbiol Immunol. 245(2):57-71.
  • Lang, J. and D. Nemazee. 2000. B cell clonal elimination induced by membrane-bound self-antigen may require repeated antigen encounter or cell competition. Eur J Immunol. 30(2):689-96.
  • Lang, J. and D. Bellgrau. 2001. Animal Models of Type 1 Diabetes. Barbara Davis Center for Childhood Diabetes Website, Chp. 3.
  • Lang, J. and D. Bellgrau. 2002. A T-cell functional phenotype common among autoimmune-prone rodent strains. Scand. J. Immunol.  55(6):546-59.
  • Ait-Azzouzene , D., P. Skog, M. Retter, V. Kouskoff,  M. Hertz, J. Lang, J. Kench, M. Chumley, D. Melamed, J. Sudaria, A. Gavin, A. Martensson, L. Verkoczy, B. Duong, J. Vela, and D. Nemazee.  2004. Tolerance-induced receptor selection: scope, sensitivity, locus specificity, and relationship to lymphocyte-positive selection. Immunol. Rev. 197:219-30.
  • Modiano, J.F., J. Sun, J. Lang, G. Vacano, D. Patterson, D. Chan, A. Franzusoff, R. Gianani, S. J. Meech, R. Duke and D. Bellgrau. 2004. Fas ligand dependent suppression of autoimmunity via recruitment and subsequent termination of activated T cells. Clin. Immuno. 112(1):54-65.
  • Lang, J., D. Bellgrau and R. Scheinman. 2004. Partial activation precedes apoptotic death in T cells harboring an IAN gene mutation. Eur. J. Immunol. 34(9):2396-406.
  • Lang, J. and D. Bellgrau. 2004. Animal models of type 1 diabetes: genetics and immunological function.  Adv. Exp med Biol. 552:91-116.
  • Verkoczy, L. D. Ait-Azzouzene, P. Skog, A. Martensson, J. Lang, B. Duong and D. Nemazee. 2005. A role for nuclear factor kappa B/rel transcription factors in the regulation of the recombinase activator genes. Immunity. 22(4):519-31.
  • R. Kupfer, J. Lang, C. Williams-Skipp, M. Nelson, D. Bellgrau, and R. I. Scheinman.  2007. Loss of an gimap/ian  Gene leads to Activation of NF-kB Through a MAPK Dependent Pathway. Mol. Immunol. 44(4):479-87. (First two authors contributed equally).
  • Jubala, C.M., A. R. Lamerato, M. Borakove, J. Lang, L. A. Gardner, D.  Coffey, K. M. Helm, J. Schaak, M. Baier, G. R. Cutter, D. Bellgrau, and J. F. Modiano. 2009. MHC-Dependent Desensitization of Intrinsic Anti-Self Reactivity. Cancer Immunol Immunother. 58(2):171-85.
  • Lang, J., N. Weiss, B. M. Freed, R. M. Torres and R. Pelanda. 2011. Generation of hematopoietic humanized mice in the newborn BALB/c-Rag2-/-IL2r-/- mouse model: a multivariable optimization approach.  Clin. Immunol.  140(1):102-116.
  • Lang J., Kelly M, Freed BM, McCarter MD, Kedl RM, Torres RM, Pelanda R. 2013. Studies of lymphocyte reconstitution in a humanized mouse model reveal a requirement of T cells for human B cell maturation. J Immunol. 190(5):2090-101.
  • Lang, J and R. Pelanda. 2013. “Human B cell development in a mouse environment,” Chapter 15 in “Humanized Mice for HIV Research.” Springer.
  • Lang, J., T. Ota, M. Kelly, P. Strauch, B.M. Freed, R.M. Torres, and R. Pelanda. 2016. Receptor editing and genetic variability in human autoreactive B cells. J. Exp. Med. 213(1):93-108.