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Contact Info

Alasdair M. Gilfillan, Ph.D.
Building 10, Rm 11C206
10 Center Drive
Bethesda MD 20892-1881
Phone: 301-496-8757
Fax: 301-480-8384
agilfillan@niaid.nih.gov

Laboratory of Allergic Diseases

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Alasdair M. Gilfillan, Ph.D.

Special Volunteer, Mast Cell Biology Section, LAD

Major Areas of Research

  • Mast cell biology
  • FcεRI-, Kit-, and GPCR-regulated secretory responses
  • Integration of signaling responses leading to mast-cell growth, differentiation, and activation
  • PI-3 kinase-regulated signaling pathways, particularly mTORC1 and mTORC2
  • Mast cell reprogramming
  • Roles of signaling molecule polymorphisms in mast cell-related disease states
 

Biography

Dr. Gilfillan received his Ph.D. from the University of Manchester, United Kingdom, and then did his postdoctoral training at Yale University Medical School. Following a number of years spent conducting pre-clinical research at Hoffmann La-Roche in the areas of allergy and inflammation, he joined the Mast Cell Biology Section of the Laboratory of Allergic Diseases in 1999. Dr. Gilfillan has a long-standing interest in signaling pathways associated with receptor-mediated activation of mast cells.

Memberships

  • American Association of Immunologists
  • American Society for Biochemistry and Molecular Biology

Editorial Boards

  • World Journal of Biological Chemistry (2010- )
  • Journal of Immunology (2008- )
  • Immunology Letters (2007- )
  • The Open Immunology Journal (2007- )
  • The Open Allergy Journal (2007- )
  • Journal of Pharmacology and Experimental Therapeutics (1994-2001)

Selected Publications

Kuehn HS, Jung MY, Beaven MA, Metcalfe DD, Gilfillan AM. Prostaglandin E2 activates and utilizes mTORC2 as a central signaling locus for the regulation of mast cell chemotaxis and mediator release. J Biol Chem. 2011 Jan 7;286(1):381-402.

Gilfillan AM, Metcalfe DD, editors. Mast cell biology: contemporary and emerging topics. Austin, TX: Landes Bioscience; 2011.

Smrž D, Iwaki S, McVicar DW, Metcalfe DD, Gilfillan AM. TLR-mediated signaling pathways circumvent the requirement for DAP12 in mast cells for the induction of inflammatory mediator release. Eur J Immunol. 2010 Dec;40:3557-61.

Kuehn HS, Rådinger M, Brown JM, Ali K, Vanhaesebroeck B, Beaven MA, Metcalfe DD, Gilfillan AM. Btk-dependent Rac activation and actin rearrangement following FceRI aggregation promotes enhanced chemotactic responses. J Cell Sci. 2010 Aug 1;123(Pt 15):2576-85.

Kataoka TR, Kumanogoh A, Bandara G, Metcalfe DD, Gilfillan AM. CD72 negatively regulates KIT-mediated responses in human mast cells. J Immunol. 2010 Mar 1;184(5):2468-75

Rådinger M, Kuehn HS, Kim MS, Metcalfe DD, Gilfillan AM. Glycogen synthase 3β activation is a prerequisite signal for cytokine production and chemotaxis in human mast cells. J Immunol. 2010 Jan 15;184(2):564-72.

Visit PubMed for a complete publication listing.

Last Updated February 13, 2013

Last Reviewed February 13, 2013