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Laboratory of Allergic Diseases

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Kirk M. Druey, M.D.

Kirk M. Druey

Chief, Molecular Signal Transduction Section, LAD

Major Areas of Research

  • Basic signaling mechanisms of G-protein-coupled receptors
  • Leukocyte trafficking in allergic inflammation
  • GPCR-induced bronchial contraction/relaxation
  • The systemic capillary leak syndrome

Program Description

The primary focus of our laboratory is to understand the signaling pathways evoked by G-protein-coupled receptors (GPCRs) and the role of specific gene protein pathways in the pathogenesis of asthma and other allergic diseases. Although therapeutic agents targeting GPCRs have long been used to treat asthma and allergies, much remains unknown about how their signaling cascades drive the immune system. Our section focuses on the role of a family of inhibitory proteins known as regulators of G protein signaling (RGS). Our goals are to understand specific GPCRs, G proteins, and RGS proteins that mediate three distinct but overlapping processes: 1) migration of leukocytes to inflammatory sites; 2) bronchial smooth muscle contraction and relaxation; and 3) vascular permeability. We use mouse models of skin and pulmonary inflammation as well as clinical studies. Of particular interest is a rare and highly unusual disorder, the systemic capillary leak syndrome. This disease is characterized by reversible episodes of hypovolemia, hypotensive shock, and ansarca, which are thought to be a result of transient endothelial hyperpermeability.


Dr. Druey obtained his M.D. from Rush Medical College in Chicago, Illinois. In 1992, following a residency in internal medicine at The New York Hospital/Cornell Medical Center, Dr. Druey became a postdoctoral fellow in the NIAID Laboratory of Immunoregulation. He joined the Laboratory of Allergic Diseases in 1997 to become chief of the Molecular Signal Transduction Section (MSTS).

Research Group

photo of reserch group members

Zhihui (Sherry) Xie, Ph.D., Staff Scientist
Tolga Barker, Ph.D. , Postdoctoral Fellow
Nariman Balenga, Ph.D., Postdoctoral Fellow
Sucharita Shankar, Ph.D., Postdoctoral Fellow
Shoko Iwaki, M.D., Ph.D., Biologist

Selected Publications

Balenga NA, Jester W, Jiang M, Panettieri RA Jr, Druey KM. Loss of regulator of G protein signaling 5 promotes airway hyperresponsiveness in the absence of allergic inflammation. J Allergy Clin Immunol. 2014 Mar 22. Epub ahead of print

Shankar SP, Wilson MS, DiVietro JA, Mentink-Kane MM, Xie Z, Wynn TA, Druey KM. RGS16 attenuates pulmonary Th2/Th17 inflammatory responses. J Immunol. 2012 Jun 15;188(12):6347-56.

Liang G, Barker T, Xie Z, Charles N, Rivera J, Druey KM. Naive T cells sense the cysteine protease allergen papain through protease-activated receptor 2 and propel TH2 immunity. J Allergy Clin Immunol. 2012 May;129(5):1377-1386.e13.

Xie Z, Ghosh CC, Patel R, Iwaki S, Gaskins D, Nelson C, Jones N, Greipp PR, Parikh SM, Druey KM. Vascular endothelial hyperpermeability induces the clinical symptoms of Clarkson disease (the systemic capillary leak syndrome). Blood. 2012 May 3;119(18):4321-32.

Damera G, Druey KM, Cooper PR, Krymskaya VP, Soberman RJ, Amrani Y, Hoshi T, Brightling CE, Panettieri RA Jr. An RGS4-mediated phenotypic switch of bronchial smooth muscle cells promotes fixed airway obstruction in asthma. PLoS One. 2012;7(1):e28504.

Visit PubMed for a complete publication listing.

Last Updated May 27, 2014