Heth R. Turnquist, Ph.D.

Heth R. Turnquist, Ph.D.

Contact

Campus: 200 Lothrop Street

Office: E1554 Biomedical Science Tower

Lab: W1500HH/II Biomedical Science Tower

Pittsburgh, PA 15261

Ph: 412-624-6695

Fax: 412-624-1172

turnquisthr@upmc.edu

Education

  • BS, South Dakota State University
  • PhD, Pathology and Microbiology, University of Nebraska

Academic Affiliation

  • Assistant Professor, Department of Surgery
  • Assistant Professor, Department of Immunology

About Research

The overall focus of my research program is the elucidation of endogenous immunoregulatory and allograft protective mechanisms that can be applied clinically for the benefit of transplant recipients.

Currently, we are highly focused on developing a translatable understanding of how cytokines, which are small cell-signaling molecules with local and systemic immunoregulatory functions, shape transplant outcomes.  Toward this goal, we employ cutting-edge research tools, including advanced imaging of clinical biopsies, computational biology, and precise cellular and molecular examinations in transgenic mouse-based transplant models.  We fully expect these methods and models will allow us to establish a precise understanding of the pro-inflammatory versus regulatory capacity of cytokines in solid organ and bone marrow transplantation.

A primary area of my research is the identification of how IL-33, acting as a cytokine secreted by immune cells or a “danger” signal when released from damaged cells, influences alloimmunity and transplant survival. IL-33 is particularly novel in that it has the potential to target both immune cells and cells of the allograft, which share expression of the IL-33 receptor.

Likewise, myeloid innate immune cells, particularly mononuclear phagocytes, have emerged as more than just critical early effectors against pathogens, but potent endogenous regulators of immune responses.  Cytokines both control myeloid immune cell generation and function and are also utilized by them to regulate immunity. We are actively developing an improved understanding of the signaling pathways that control myeloid cell responses to cytokines, as well as shape their cytokine production and related immunoregulatory or stimulatory functions.

Publications

Selected Publications

Rosborough BR, Mathews LR, Matta BM, Liu Q, Raïch-Regué D, Thomson AW, and Turnquist HR. Cutting edge: Flt3 ligand mediates STAT3-independent expansion but STAT3-dependent activation of myeloid-derived suppressor cells. 2014. Journal of Immunology 192(8): 3470-3473.

Stenger E, Rosborough BR, Mathews L, Ma H, Mapara M, Thomson AW and Turnquist HR. IL-12hi Rapamycin-Conditioned Dendritic Cells Mediate IFN-γ-Dependent Apoptosis of Alloreactive CD4+ T Cells In Vitro and Reduce Lethal Graft-versus-Host Disease. 2014.  Biology of Blood and Marrow Transplantation 20(2): 192-201.

Rosborough BR, Raïch-Regué D, Matta BM, Lee K, Gan B, DePinho RA, Hackstein H, Boothby M, Turnquist HR, and Thomson AW. Murine dendritic cell rapamycin-resistant and rictor-independent mTOR controls IL-10, B7-H1 and regulatory T cell induction. 2013. Blood. 121: 3619-30.

Turnquist HR, Zhoa Z, Rosborough BR, Liu Q, Castellaneta A, Isse K, Wang Z, Lang M, Beer Stolz D, Zheng XX, Demetris AJ, Liew FY, Wood KJ, and Thomson AW. IL-33 expands suppressive CD11b+ Gr-1int and regulatory T cells (Treg), including ST2L+ Foxp3+ cells, and mediates Treg-dependent promotion of cardiac allograft survival. 2011. Journal of Immunology. 187(9): 4598-610. 

Turnquist HR, Cardinal JS, Macedo C, Rosborough BR, Sumpter TL, Geller DA, Metes D, and Thomson AW. mTOR and GSK-3 shape the CD4+ T cell stimulatory and differentiation capacity of myeloid DC following exposure to LPS. 2010. Blood. 115: 4758-4769.

Turnquist HR, Sumpter TL, Tsung A, Zahorchak AF, Nakao A, Nau GJ, Liew FY, Geller DA, and Thomson AW.  IL-1b-driven ST2L expression promotes maturation resistance in rapamycin-conditioned dendritic cells. 2008. Journal of Immunology. 181: 62-72.

Turnquist HR, Raimondi R, Zahorchak AF, Fischer R, Wang Z, and Thomson AW. Rapamycin-conditioned dendritic cells are poor stimulators of allogeneic CD4 T cells, but enrich for antigen-specific Foxp3+ T regulatory cells and promote organ transplant tolerance. 2007. Journal of Immunology. 178: 7018 –7031.

Research Interests

  • Cytokine immunobiology
  • Innate immune cell regulation of immunity and tolerance
  • Transplant immunology
  • Alarmins
  • Characterization and application of regulatory immune cells in transplantation