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Andrew D. Luster, MD, PhD

Persis, Cyrus and Marlow B. Harrison Professor of Medicine, Department of Medicine, Harvard Medical School

Chief, Rheumatology, Allergy and Immunology, Massachusetts General Hospital

Contact Info

Andrew Luster
Massachusetts General Hospital
Building 149

Charlestown, MA, 02129
Mailstop: Room 8301
Phone: 617-726-5710
Fax: 617-726-5651


Diane Qualters
Executive Assistant
Center for Immunology and Inflammatory Diseases
Massachusetts General Hospital
Building 149
13th Street
Charlestown, MA, 02129
Mailstop: #8301
Phone: 617-724-6147
Fax: 617-726-5651

DF/HCC Program Affiliation

Cancer Immunology

Research Abstract

Dr. Lusterís 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 Dr. Lusterís laboratory focuses on understanding the role of chemokines and lipid chemoattractant receptors in controlling the trafficking of leukocytes in vivo. His laboratory uses gene-targeted and transgenic overexpressing mouse strains and inhibitory monoclonal antibodies to study the role of individual chemokines and chemoattractant receptors in mouse models of disease. The laboratory also studies the regulation of chemokine production in vivo in both humans and mice since this is a critical determinant of their role in a given biological response. The members of the laboratory believe that a greater understanding of the chemokine superfamily will lead to novel therapies aimed at inhibiting a dysregulated host response in autoimmune and allergic conditions as well as augmenting the host response to tumor cells, infectious agents and vaccines. The laboratory also studies how the innate immune system controls the adaptive immune system through collaborative interactions between Toll-like receptors (TLRs) and scavenger receptors.


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