Affiliation(s):
BC Cancer Agency
Location:
Terry Fox Laboratory
Academic Backgrounds:
  • BSc, University of Tokyo, Tokyo, Japan, Biochemistry. 1968
  • PhD, University of British Columbia, Vancouver, BC, Immunology. 1976
  • Postdoctoral Fellow, University of British Columbia, Microbiology, 1977
  • Postdoctoral Fellow, MRC Laboratory of Molecular Biology, Cambridge, England. 1979
Selected Publications
  • Halim TYF, Steer CA, Matha L, Gold MJ, Antignano F, McNagny KM & Takei F. Group 2 innate lymphoid cells are critical for the initiation of adaptive T helper 2 cell mediated allergic lung inflammation. Immunity 40: 425-435, 2014.
  • Gold MJ, Antignano F, Halim TYF, Blanchet M-R, Zaph C, Takei F & McNagny KM. Group 2 innate lymphoid cells facilitate sensitization to local but not systemic Th-2-inducing allergen exposures. J Allergy Clin Immunol 133: 1142-1148, 2014.
  • Halim TYF & Takei F. Isolation and characterization of mouse innate lymphoid cells. In Vivo Assays for Mouse Lymphocyte Function., John Wiley & Sons, Inc., Curr Protoc Immunol 106: 3.25.1-3.25.13, 2014.
  • Halim TY, MacLaren A, Romanish MT, Gold MJ, McNagny KM, Takei F. Retinoic-acid-receptor-related orphan nuclear receptor alpha is required for natural helper cell development and allergic inflammation. Immunity. 2012 Sep 21;37(3):463-74.
  • Halim TY, Krauss RH, Sun AC, Takei F. Lung natural helper cells are a critical source of Th2 cell-type cytokines in protease allergen-induced airway inflammation. Immunity. 2012 Mar 23;36(3):451-63.
  • Warner K, Luther C, Takei F. Lymphoid progenitors in normal mouse lymph nodes develop into NK cells and T cells in vitro and in vivo. Exp Hematol. 2012 May;40(5):401-6.
  • Takei F. LAK cell therapy of AML: not to be lost in translation. Exp Hematol. 2011 Nov;39(11):1045-6.
  • Luther C, Warner K, Takei F. Unique progenitors in mouse lymph node develop into CD127+ NK cells: thymus-dependent and thymus-independent pathways. Blood. 2011 Apr 14;117(15):4012-21.
  • Mace EM, Zhang J, Siminovitch KA, Takei F. Elucidation of the integrin LFA-1-mediated signaling pathway of actin polarization in natural killer cells. Blood. 2010 Aug 26;116(8):1272-9.
  • Kastrukoff LF, Lau AS, Takei F, Smyth MJ, Jones CM, Clarke SR, Carbone FR. Redundancy in the immune system restricts the spread of HSV-1 in the central nervous system (CNS) of C57BL/6 mice. Virology. 2010 May 10;400(2):248-58.
  • Mace EM, Zhang J, Siminovitch KA, Takei F. Elucidation of the integrin LFA-1-mediated signaling pathway of actin polarization in natural killer cells. Blood. 2010 Aug 26;116(8):1272-9.
  • Haddad EA, Senger LK, Takei F. An accessory role for B cells in the IL-12-induced activation of resting mouse NK cells. J Immunol. 2009 Sep 15;183(6):3608-15.
  • Alcón VL, Luther C, Balce D, Takei F. B-cell co-receptor CD72 is expressed on NK cells and inhibits IFN-gamma production but not cytotoxicity. Eur J Immunol. 2009 Mar;39(3):826-32.
  • Rouhi A, Lai CB, Cheng TP, Takei F, Yokoyama WM, Mager DL. Evidence for high bi-allelic expression of activating Ly49 receptors. Nucleic Acids Res. 2009 Jul 15.
  • Alcón VL, Luther C, Balce D, Takei F. B-cell co-receptor CD72 is expressed on NK cells and inhibits IFN-gamma production but not cytotoxicity. Eur J Immunol. 2009 Mar;39(3):826-32.
  • Mace EM, Monkley SJ, Critchley DR, Takei F. A dual role for talin in NK cell cytotoxicity: activation of LFA-1-mediated cell adhesion and polarization of NK cells. J Immunol. 2009 Jan 15;182(2):948-56.
  • Veinotte LL, Halim TY, Takei F. Unique subset of natural killer cells develops from progenitors in lymph node. Blood. 2008 Apr 15;111(8):4201-8.
  • Wilson EB, Parachoniak CA, Carpenito C, Mager DL, Takei F. Expression of murine killer immunoglobulin-like receptor KIRL1 on CD1d-independent NK1.1(+) T cells. Immunogenetics. 2007 Aug;59(8):641-51.
Research:
  • Molecular immunology of lymphocyte surface molecules
  • Cancer
  • Cell-cell interactions
  • Molecular Immunology. Our research is concerned with lymphocyte surface molecules that play important roles in the immune system. We currently study two groups of molecules. The first group of molecules is the Ly-49 family of natural killer (NK) cell receptors. NK cells are capable of killing a wide range of tumor cells and virus-infected cells, but spare normal cells. The precise mechanisms by which NK cells distinguish tumor cells from normal cells and kill the former are still unknown. Recent studies have shown that the Ly-49 family of receptors on NK cells interact with the Major Histocompatibility Complex (MHC) molecules on target cells and inhibit NK cell cytotoxicity, providing protection of normal cells expressing MHC molecules from NK cells. Through gene cloning studies, we have demonstrated that Ly-49 is encoded by a highly polymorphic gene complex. We have also determined the ligand binding specificities and functions of some of the Ly-49 family members. We are currently investigating the molecular interaction between Ly-49 and MHC, and will further determine the role of Ly-49 in NK cell functions. These studies will help us understand how NK cells kill tumor cells but not normal cells. The second group of molecules of our interest are cell adhesion molecules ICAMs and LFA-1. These molecules are expressed on the surface of lymphocytes and other cell types. They interact with each other and mediate direct cell-cell binding. These cell adhesion molecules are directly involved in the migration of lymphoid cells into inflamed tissues.They also mediate appropriate cellular interactions that are required for the activation of resting lymphocytes as well as effector functions of activated lymphocytes. The expression and functions of these cell adhesion molecules are strictly regulated, allowing lymphocytes to adhere to other cells only when it is needed. Our goal is to elucidate the mechanisms that regulate the functions of these molecules. By introducing modified cDNA encoding these adhesion molecules into target cells, as well as by generating recombinant adhesion molecules, we are identifying genes and proteins involved in the regulation of these molecules. Our understanding of the regulation of these cell adhesion molecules will have important implications to the treatment of various immunological and inflammatory diseases.