Marc Bix, PhD

Mark Bix, PhD

Assistant Member, St. Jude Faculty
Affiliated Assistant Professor, Department of Molecular Sciences, University of Tennessee Health Science Center College of Medicine

Departments

Immunology

Contact Information

Mark Bix, PhD
Immunology
MS 351, Room E7064
St. Jude Children's Research Hospital
262 Danny Thomas Place
Memphis, TN 38105-3678
Email: mark.bix@stjude.org
Phone: (901) 595-5459
FAX: (901) 595-3107

Education

BS - Brandeis University, Waltham, MA (1985)
PhD - Massachusetts Institute of Technology, Cambridge (1993)


Research Interests

Research in the Bix lab is focused on the developmental regulation of cytokine gene expression within T cells, with a particular focus on the TH2 locus encoding interleukins 4, 13 and 5 — key orchestrators of the immune response. The lab has undertaken the molecular genetic dissection of regulatory elements at the TH2 locus to understand how distinct gene transcriptional states of silence and permissiveness are targeted, established and maintained during effector T cell development. The lab is also applying a combination of classical genetic and genomic approaches to identify novel immune response genes, including those acting in vitro to modify effector T cell differentiation as well as in in vivo mouse models, to modify the responses to infectious agents (bacteria, fungi and worms) and inducers of autoimmune disease (systemic lupus erythematosus).


Selected Publications

Van Stry M, Oguin T, Cheloufi S, Vogel P, Watanabe M, Pillai MR, Dash P, Thomas P, Hannon GJ, Bix M. Enhanced susceptibility to influenza A virus of Ago1/3 double null mice. J Virol 86(8):4151-57, 2012.

Pillai MR, Bix M. Evolution of IL4 and pathogen antagonism. Growth Factors 29(4)153-60, 2011.

Van Stry M, Bix M. Explaining discordant coordination. Nat Immunol 12(1):16-17, 2011.

Koyanagi M, Kerns JA, Chung L, Zhang Y, Brown S, Moldoveanu T, Malik HS, Bix M. Diversifying selection and functional analysis of interleukin-4 suggests antagonism-driven evolution at receptor-binding interfaces. BMC Evol Biol 10:223, 2010.

Okamoto M, Van Stry M, Chung L, Koyanagi M, Sun X, Suzuki Y, Ohara O, Kitamura H, Hijikata A, Kubo M, Bix M. Mina, an Il4 repressor, controls T helper type 2 bias. Nat Immunol 10:872-U98, 2009.

Baguet A, Sun X, Arroll T, Krumm A, Bix M. Intergenic transcription is not required in TH2 cells to maintain histone acetylation and transcriptional permissiveness at the Il4-Il13 locus. Journal of Immunology 175:8146-8153, 2005.

Koyanagi M, Baguet A, Martens J, Margueron R, Jenuwein T, Bix M. EZH2 and H3-tri-methyl lysine 27 associated with Il4 and Il13 gene silencing in TH1 cells. J Biol Chem 280:31470-31477, 2005.

Bix M, Kim S, Rao A. Opposites attract: cytokine transcription in differentiating T cells. Science 308:1563-1565, 2005.

Baguet A, Epler J, Wa-Wen K, Bix M. A Leishmania major resistance locus identified by interval-specific congenic mapping of a TH2 bias controlling QTL. J Exp Med 200:1605-1611, 2004.

Baguet A, Bix M. Chromatin landscape dynamics of the Il4-Il13 locus during T helper 1 and 2 development. Proc Natl Acad Sci USA 101:11410-11415, 2004.

Locksley RM, Pingel S, Lacy D, Wakil AE, Bix M, Fowell DJ. Susceptibility to infectious diseases: Leishmania as a paradigm. J Infect Dis 179 (Suppl 2):S305-S308, 1999.

Locksley RM, Fowell D, Shinkai K, Wakil AE, Lacy D, Bix M. Development of CD4 effector T cells and susceptibility to infectious diseases. Adv Exp Med Biol 452:45-52, 1998.

Bix M, Wang Z, Thiel B, Schork N, Locksley R. Genetic regulation of commitment to interleukin 4 production by a CD4( ) T cell-intrinsic mechanism. J Exp Med 188:2289-1199, 1998.

Bix M, Locksley R. Independent and epigenetic regulation of interleukin-4 alleles in CD4 T cells. Science 281:1352-1354, 1998.

Brossay L, Tangri S, Bix M, Cardell S, Locksley R, Kronenberg M. CD1 autoreactive T cells have diverse patterns of reactivity to CD1 targets. J Immun 160:3681-3688, 1997.

Williams O, Tanaka Y, Bix M, Murdjeva M, Littman DR, Kioussis D. Inhibition of thymocyte negative selection by T cell receptor antagonist peptides. Eur J Immun 26:532-538, 1996.

Bix M, Locksley R. Natural T cells: cells that co-express NKRP-1 and TCR. J Immun 155:1020-1022, 1995.

Bix M, Coles M, Raulet D. Positive selection of V-beta 8 CD4-8- thymocytes by class I molecules expressed by hematopoietic cells. J Exp Med 178:901-908, 1992.

Bix M, Raulet D. Inefficient positive selection of T-cells directed by hematopoietic cells. Nature 359: 330-333, 1992.

Bix M, Raulet D. Functionally conformed free class I heavy chains exist on the surface of beta-2 microglobulin negative cells. J Exp Med 176: 829-834, 1992.

Correa I, Bix M, Liao NS, Zijlstra M, Jaenisch R, Raulet D. Most gamma delta T cells develop normally in beta 2-microglobulin-deficient mice. Proc Natl Acad Sci USA 89:653-657, 1992.

Raulet D, Liao NS, Correa I, Bix M. Lymphocyte development in mice deficient for MHC class I expression. Adv Exp Med Biol 323:67-72, 1992.

Liao NS, Bix M, Zijlstra M, Jaenisch R, Raulet D. MHC class I deficiency: susceptibility to natural killer (NK) cells and impaired NK activity. Science 253:199-202, 1991.

Raulet DH, Spencer DM, Hsiang YH, Goldman JP, Bix M, Liao NS, Zijistra M, Jaenisch R, Correa I. Control of gamma delta T-cell development. Immunol Rev 120:185-204, 1991.

Bix M, Liao NS, Zijlstra M, Loring J, Jaenisch R, Raulet D. Rejection of class I MHC-deficient haemopoietic cells by irradiated MHC-matched mice. Nature 349:329-331, 1991.

Zijlstra M, Bix M, Simister NE, Loring JM, Raulet D, Jaenisch R. Beta 2-microglobulin deficient mice lack CD4-8 cytolytic T cells. Nature 344:742-746, 1990.

Last update: October 2012