Trevor Burt, MD

TitleAssistant Professor
InstitutionUniversity of California San Francisco
Address35 Medical Center Way
San Francisco CA 94143
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    Collapse Biography 
    Collapse Education and Training
    Harvard UniversityM.D.2002School of Medicine
    Collapse Awards and Honors
    American Society for Clinical Investigation2014Young Physician Scientist Award
    Burroughs Wellcome Fund2014  - 2018Preterm Birth Initiative Award - Fetal Immune Activation and Lineage Switching in Preterm Birth
    University of California San Francisco2014  - 2015A Novel Approach to Study Human Fetal T Cell Differentiation and Function in vitro using iPS cells.
    UCSF-Gladstone Institute of Virology and Immunology Center for AIDS Research (CFAR) 2010  - 2011“Outside the Box” AIDS Vaccine Discovery Award
    Pediatric Scientist Development Program (PSDP)2006  - 2009PSDP Fellowship
    Sarnoff Cardiovascular Research Foundation2000  - 2001Sarnoff Fellowship

    Collapse Overview 
    Collapse Overview
    I am an practicing neonatologist and also a lab-based basic/translational researcher with interests in development and function of the fetal and neonatal immune system. I am especially interested in how the developmental state of the immune system affects fetal and newborn susceptibility to infections. Related to this, I am also interested in how the immune system contributes to the pathogenesis of preterm labor.


    Newborn infants are susceptible to serious infections by a wide range of pathogens, especially infants who are born prematurely. This has generally been interpreted to mean that the developing immune system is inactive, ineffective, or uneducated. To the contrary, the human fetal immune system is highly functional, but its primary function appears to be establishing and maintaining immune tolerance.

    We focus on two main areas of developmental immunology: (1) how the human fetal immune system is specially adapted to prevent, terminate, or down-regulate immune responses in order to create tolerance; and (2) how the transition from fetal to adult immunity influences neonatal responses to antigen challenge and infection. These two areas of interest are united by the hypothesis that, due to persistent tolerogenic fetal developmental programs, the newborn immune system is prone to be tolerant of the stimuli it encounters. Therefore, rather than mounting an adaptive immune response that would lead to clearing an infection, the infant tends to mount responses that may lead to tolerance. We are committed to employing translational strategies to understand the basis of fetal immune tolerance by studying basic molecular and cellular phenomena, with the goal of ultimately utilizing basic discoveries to inform patient-oriented research. Current projects in the lab include:

    (1) Molecular regulation of fetal T cell differentiation and function. Fetal and adult T cells appear to arise from unique, developmentally restricted hematopoietic stem cell (HSC) populations, resulting in distinct immunologic functions and gene-expression signatures. Utilizing molecular genetic approaches in vitro and in humanized mouse models, we are studying factors that direct the differentiation of, and mediate functional responses in tolerogenic fetal T cells. The goal of these studies is to better understand mechanisms of fetal tolerance, and to ultimately use these findings to generate novel therapeutic approaches for use in settings where broken tolerance leads to disease, such as autoimmune disease or transplant rejection. We are concurrently developing in vitro models utilizing induced pluripotent stem cell (iPSc) technology to study the process of T cell differentiation.

    (2) The influence of fetal T cells on human neonatal immunity. Based on our findings, we hypothesize that newborns are in a state of transition between dominance of tolerogenic fetal T cells and immunogenic adult T cells. If so, the degree to which this transition has occurred at the time of birth would influence how neonates respond to antigenic challenge and infection. We have developed assays to measure the relative abundance of fetal and adult T cell gene expression in newborns. Utilizing these assays, we have shown that there is striking variability in the degree of immune maturation at birth. We are currently engaged in several translational projects to investigate the potential importance of this finding in various settings, including: (1) response to neonatal vaccination; (2) susceptibility to childhood viral infections and asthma; and (3) the pathogenesis of preterm labor.

    Collapse Research 
    Collapse Research Activities and Funding
    Understanding Molecular Pathways for Fetal T Cell Development and Function
    NIH/NIAID R21AI120032Jul 1, 2015 - Jun 30, 2017
    Role: Principal Investigator
    Defining Transition from Fetal to Adult T Cell Predominance in the Human Fetus
    NIH/NICHD K08HD067295Feb 10, 2011 - Jan 31, 2016
    Role: Principal Investigator

    Collapse ORNG Applications 
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    Collapse Bibliographic 
    Collapse Publications
    Publications listed below are automatically derived from MEDLINE/PubMed and other sources, which might result in incorrect or missing publications. Researchers can login to make corrections and additions, or contact us for help.
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    1. Kattah MG, Milush JM, Burt T, McCabe RP, Whang MI, Ma A, Mahadevan U. Anti-TNF and thiopurine therapy in pregnant IBD patients does not significantly alter a panel of B-cell and T-cell subsets in 1-year-old infants. Clin Transl Gastroenterol. 2018 Apr 03; 9(4):143. PMID: 29618720.
      View in: PubMed
    2. Bronevetsky Y, Burt T, McCune JM. Lin28b Regulates Fetal Regulatory T Cell Differentiation through Modulation of TGF-ß Signaling. J Immunol. 2016 12 01; 197(11):4344-4350. PMID: 27793996.
      View in: PubMed
    3. Seu L, Ortiz GM, Burt T, Deeks SG, Martin JN, McCune JM. Levels of circulating myeloid subpopulations and of heme oxygenase-1 do not predict CD4(+) T cell recovery after the initiation of antiretroviral therapy for HIV disease. AIDS Res Ther. 2014; 11:27. PMID: 25180041; PMCID: PMC4150425.
    4. Krow-Lucal ER, Kim CC, Burt T, McCune JM. Distinct functional programming of human fetal and adult monocytes. Blood. 2014 Mar 20; 123(12):1897-904. PMID: 24518760; PMCID: PMC3962163.
    5. Burt T. Fetal regulatory T cells and peripheral immune tolerance in utero: implications for development and disease. Am J Reprod Immunol. 2013 Apr; 69(4):346-58. PMID: 23432802; PMCID: PMC3951896.
    6. Seu L, Burt T, Witte JS, Martin JN, Deeks SG, McCune JM. Variations in the heme oxygenase-1 microsatellite polymorphism are associated with plasma CD14 and viral load in HIV-infected African-Americans. Genes Immun. 2012 Apr; 13(3):258-67. PMID: 22048453; PMCID: PMC3330188.
    7. Mold JE, Venkatasubrahmanyam S, Burt T, Michaëlsson J, Rivera JM, Galkina SA, Weinberg K, Stoddart CA, McCune JM. Fetal and adult hematopoietic stem cells give rise to distinct T cell lineages in humans. Science. 2010 Dec 17; 330(6011):1695-9. PMID: 21164017; PMCID: PMC3276679.
    8. Burt T, Seu L, Mold JE, Kappas A, McCune JM. Naive human T cells are activated and proliferate in response to the heme oxygenase-1 inhibitor tin mesoporphyrin. J Immunol. 2010 Nov 01; 185(9):5279-88. PMID: 20921523; PMCID: PMC3314532.
    9. Mold JE, Michaëlsson J, Burt T, Muench MO, Beckerman KP, Busch MP, Lee TH, Nixon DF, McCune JM. Maternal alloantigens promote the development of tolerogenic fetal regulatory T cells in utero. Science. 2008 Dec 05; 322(5907):1562-5. PMID: 19056990; PMCID: PMC2648820.
    10. Burt T, Agan BK, Marconi VC, He W, Kulkarni H, Mold JE, Cavrois M, Huang Y, Mahley RW, Dolan MJ, McCune JM, Ahuja SK. Apolipoprotein (apo) E4 enhances HIV-1 cell entry in vitro, and the APOE epsilon4/epsilon4 genotype accelerates HIV disease progression. Proc Natl Acad Sci U S A. 2008 Jun 24; 105(25):8718-23. PMID: 18562290; PMCID: PMC2438419.
    11. Napolitano LA, Burt T, Bacchetti P, Barrón Y, French AL, Kovacs A, Anastos K, Young M, McCune JM, Greenblatt RM. Increased circulating interleukin-7 levels in HIV-1-infected women. J Acquir Immune Defic Syndr. 2005 Dec 15; 40(5):581-4. PMID: 16284535; PMCID: PMC3119025.
    12. Hirsch GM, Kearsey J, Burt T, Karnovsky MJ, Lee T. Medial smooth muscle cell loss in arterial allografts occurs by cytolytic cell induced apoptosis. Eur J Cardiothorac Surg. 1998 Jul; 14(1):89-96; discussion 96-7. PMID: 9726621.
      View in: PubMed
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