Andrew D. Luster
Center for Immunology and Inflammatory Diseases
Division of Rheumatology, Allergy and Immunology
Massachusetts General Hospital
Building 149, 13th Street, Room 8301
Charlestown, MA 02129
Tel: 617-726-5710
Fax: 617-726-5651
email: aluster@mgh.harvard.edu
14 Postdoctoral Fellows
My laboratory studies the basic biology and pathobiology of chemokines (chemotactic cytokines) and lipid chemoattractants. Chemokines are the largest family of cytokines and control the movement of leukocytes in development, homeostasis, and response to infection and inflammation by binding to specific G protein-coupled seven transmembrane cell surface receptors (GPCRs) on leukocytes.
Research in my laboratory focuses on understanding the role of chemokines and lipid chemoattractants and their chemoattractant receptors in controlling the trafficking of leukocytes in vivo. We use gene-targeted and transgenic mouse strains to study the role of individual chemokines and chemoattractant receptors in innate and adaptive immunity and make use of mouse models of infectious and inflammatory diseases. We also study the regulation of chemokine production in vivo since this is a critical determinant of their role in a given biological response. We have a particular interest in the role of innate immune receptors, such as toll-like receptors (TLR) and scavenger receptors, in regulating chemokine production and cell migration in vivo. We are also interested in structure-function relationships of chemokines and their receptors as well as the molecular mechanism of chemokine signal transduction, which are important questions relevant to chemotaxis and immune cell trafficking in health and disease.
Understanding the function of the chemokine superfamily will provide key insights into the regulation of the immune response as cell trafficking and location determine cell fate and function. In addition, understanding chemokine biology will lead to novel therapies aimed at augmenting the host response to tumor cells, infectious agents and vaccines. It will also allow the inhibition of a dysregulated host response in autoimmune, allergic and inflammatory conditions.
References:
- El Khoury J, Toft M, Hickman S, Means TK, Terada K, Geula C, Luster AD. CCR2 deficiency impairs microglial accumulation and accelerates progression of Alzheimer’s-like disease. Nat Med. 2007; 13: 432-438.
- Tager AM, LaCamera P, Shea BS, Campanella GK, Selman M, Zhao Z, Polosukhin V, Wain J, Karimi-Shah BA, Kim ND, Hart WK, Pardo A, Blackwell TS, Xu Y, Chun J, Luster AD. The lysophosphatidic acid receptor LPA1 links pulmonary fibrosis to lung injury by mediating fibroblast recruitment and vascular leak. Nat Med. 2008; 14: 45-54.
- Campanella GS, Tager AM, El Khoury JK, Thomas SY, Abrazinski TA, Manice LA, Colvin RA, Luster AD. Chemokine receptor CXCR3 and its ligands CXCL9 and CXCL10 are required for experimental cerebral malaria. Proc Natl Acad Sci. 2008; 105; 4814-4819.
- Medoff BD, Thomas SY, Luster AD. T cell trafficking in allergic asthma: the ins and outs. Annual Review of Immunology 2008; 26: 205-232.
- Bromley SK, Mempel TR, Luster AD. Orchestrating the orchestrators – chemokine control of T cell trafficking. Nature Immunology 2008 (Invited, in press).
Immunology webpage updated 12/02/2009