Francisco Quintana, PhD

2010 DICP Faculty Fellowship Alumni

FRANCISCO QUINTANA, Ph.D., Associate Professor of Neurology, Harvard Medical School, Brigham and Women’s Hospital

Mentor: Howard Weiner, M.D., Robert L. Kroc Professor of Neurology, Harvard Medical School, Brigham and Women’s Hospital/Harvard Institutes of Medicine

Department Chair: Martin Samuels M.D., Head of the Department of Neurology, Brigham and Women’s Hospital; Professor of Neurology, Harvard Medical School

Project Title: "Role of the transcription factor aryl hydrocarbon receptor (AHR) in human regulatory T cells"

Project Description:

Autoimmune diseases such as multiple sclerosis (MS), type I diabetes mellitus and rheumatoid arthritis result from a dysregulated immune response directed against self-tissue.  In MS, the immune system targets the central nervous system (CNS), leading to progressive neurological dysfunction. The activity of the immune system is normally under the control of a specialized class of T cells termed regulatory T cells (Treg).  Treg deficits have been found in several autoimmune diseases, including MS.  Based on this Treg deficit, the induction of functional Treg is viewed as a therapeutic approach for MS and other autoimmune disorders. We have recently found that the ligand-activated transcription factor aryl hydrocarbon receptor (AHR) controls the development of Treg. Moreover, we found that the non-toxic AHR ligand 2-(1’H-indole-3’-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) induces functional Treg cells that suppress disease progression in experimental models of autoimmunity.  Thus, non-toxic AHR ligands represent a new tool for the therapeutic induction of Treg in autoimmune diseases. In this project, we will investigate the role of AHR in the induction of human Treg.  If successful, our project will pave the way for the use of non-toxic AHR ligands for the treatment of human autoimmune disorders. First, what is the effect of AHR activation by different ligands on human Treg? Second, can AHR activation be used to induce functional Treg from MS patients?

Biography:

Francisco J. Quintana, PhD is an Associate Professor of Neurology at the Center for Neurologic Diseases, Department of Neurology at the Brigham and Women’s Hospital.  Dr. Quintana, a graduate of the University of Buenos Aires (1999, Argentina), obtained his PhD in immunology at the Weizmann Institute of Science (2004, Israel), where he worked under the supervision of Prof. Irun Cohen in the development of antigen arrays and DNA vaccines for the diagnosis and therapy of autoimmune disorders. Dr. Quintana then was a postdoc of Prof. Irun Cohen and Yechiel Shai at the Weizmann Institute of Science, where he studied the structural aspects of the T cell receptor.

In 2005, Dr. Quintana moved to the Center of Neurologic Diseases in Boston, to work in the identification of biomarkers for the staging of multiple sclerosis and in the study of molecular pathways that control the immune response, using several experimental models including zebrafish, mouse and human cells. 

In 2009, Dr. Quintana moved to his current position.  Dr. Quintana’s research interests include mechanisms of immunoregulation, innate immunity and systems immunology approaches for the staging and monitoring of autoimmune disorders.