Daniel Robert Goldstein, MBBS

Professor of Medicine (Cardiology) and of Immunobiology

Departments & Organizations

Immunobiology: HTI

Immunology and Immunotherapy

Internal Medicine: Cardiovascular Medicine: Heart Failure & Transplant; Yale Cardiovascular Research Center

Office of Student Research

Vascular Biology and Therapeutics Program

Yale Center for Advanced Heart Failure, Mechanical Circulatory Support, and Heart Transplantation

Yale Combined Program in the Biological and Biomedical Sciences (BBS): Immunology

Yale Medical Group

Biography

As a transplant physician, I have investigated the mechanisms and consequences of innate immune activation after organ transplantation. My laboratory was the first to demonstrate that Toll like receptor signaling via MyD88 accelerated the tempo of acute transplant rejection (JCI, 2003, AJT, 2004) and impaired transplant tolerance (JI, 2006, JASN, 2008). These were some of the first studies to show that Toll like receptors activate inflammation in sterile in vivo models. The activators of the innate immune system after transplantation have remained elusive. We recently discovered that haptoglobin stimulates innate immunity to induce inflammation after organ transplantation (JCI, 2012). As a result of our work some laboratories and pharmaceutical companies are targeting innate immune pathways to reduce inflammation after organ transplantation.

I am also interested in how aging impacts immunity, initially to determine if older transplant recipients exhibit altered immune responses to transplantation. My laboratory challenged the paradigm that declining immune function is responsible for age-associated disorders. In murine viral infection models, we determined that exaggerated IL-17 production by NKT cells induces lethal immune pathology (Cell Host and Microbe, 2009). In murine vascular models, we demonstrated that elevated inflammatory responses by vascular smooth muscle cells may predispose to atherosclerosis (ATVB, 2012). Finally, in murine transplant models we documented that enhanced responses by naïve CD8+ T cells may impair immune tolerance with aging (JI, 2011). In sum, we have made innovative findings, challenging current paradigms, that elevated immune responses explain age-associated phenotypes.

Education & Training

MBBS University of London (1992)
Resident Johns Hopkins Bayview Medical Center
Fellow University of Alabama- Birmingham
Fellow University of Alabama- Birmingham
Board Certification AB of Internal Medicine (2010)
Board Certification AB of Internal Medicine (2000)
Board Certification AB of Internal Medicine (1996)

Honors & Recognition

  • MemberAmerican Society of Clinical Investigation (2010)

  • Basic Scientist AwardAmerican Society of Tansplantation (2007)

  • Established Investigator AwardAmerican Heart Association (2009)

  • NIA Mid Career Development AwardNational Institute on Aging (2008)

  • Sir William Osler Young Investigator Award, Interurban Clinical Club (2012)

Professional Service

  • NIH Study Section TTT NIH (2008 - 2012)

  • Section Editor, Journal of Immunoloy (2009 - 2013)

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