In his previous role at University of Pittsburgh, Dr. Reinhart established and led a research program on HIV/AIDS and other infectious diseases that achieved more than $7 million in federal funding. At Saint Mary's, he initiated the Regenerative Medicine Workshop.
Areas of Expertise (4)
Harvard T.H. Chan School of Public Health: Sc.D., Cancer Biology 1992
My doctoral studies were conducted for the first three years at the Harvard School of Public Health and for the final three years at the Stanford University School of Medicine. The focus of those studies was on immunodeficiency-inducing viruses, particularly feline leukemia virus (FeLV) but also human immunodeficiency virus type 1 (HIV-1). This work revealed that the immunodeficiency-inducing strain of FeLV failed to establish superinfection interference, a phenomenon by which retroviruses protect the cells that they infect from further infection by the same strain of virus. Failure to establish superinfection interference is associated with cytopathic effect, at least in vitro. These findings were published in The Journal of Virology. Dr. James Mullins was my doctoral mentor.
Duquesne University: Master’s Degree, Leadership and Liberal Studies 2009
Hamline University: Bachelor’s Degree, Biology 1986
Recent Media Appearances (2)
University of Pittsburgh Department of Immunology
Winona Daily News online
Saint Mary’s University’s first-ever dean of sciences and health professions officially began work earlier this month, representing a continuing focus on the sciences at the university backed by a multi-million dollar building rising on the Winona campus.
Saint Mary’s University names Reinhart as dean of sciences and health professions
Saint Mary's University News online
As part of its bold new vision for excellence in the sciences, Saint Mary’s University of Minnesota has named Dr. Todd Reinhart to the newly created position of dean of sciences and health professions.
Recent Articles (3)
Hideho Okada, Pawel Kalinski, Ryo Ueda, Aki Hoji, Gary Kohanbash, Teresa E. Donegan, Arlan H. Mintz, Johnathan A. Engh, David L. Bartlett, Charles K. Brown, Herbert Zeh, Matthew P. Holtzman, Todd A. Reinhart, Theresa L. Whiteside, Lisa H. Butterfield, Ronald L. Hamilton, Douglas M. Potter, Ian F. Pollack, Andres M. Salazar, and Frank S. Lieberman
A phase I/II trial was performed to evaluate the safety and immunogenicity of a novel vaccination with α-type 1 polarized dendritic cells (αDC1) loaded with synthetic peptides for glioma-associated antigen (GAA) epitopes and administration of polyinosinic-polycytidylic acid [poly(I:C)] stabilized by lysine and carboxymethylcellulose (poly-ICLC) in HLA-A2+ patients with recurrent malignant gliomas. GAAs for these peptides are EphA2, interleukin (IL)-13 receptor-α2, YKL-40, and gp100.
Shulin Qin, Beth A. Fallert Junecko, Anita M. Trichel, Patrick M. Tarwater, Michael A. Murphey-Corb, Denise E. Kirschner, Todd A. Reinhart
Infection by HIV-1 frequently leads to pulmonary complications, including alterations to local immune environments. To better understand these alterations, we have examined in detail the patterns and levels of expression of chemokine, cytokine, and chemokine receptor mRNAs in lung tissues from 16 uninfected or simian immunodeficiency virus (SIV)/DeltaB670 infected cynomolgus macaques at different stages of infection. Among the most up-regulated immune genes were interferon (IFN)-γ, IFN-γ-inducible CXCR3 ligands, and CCR5 ligands, as well as the cognate chemokine receptors. These changes were greatest in animals with clear Pneumocystis carinii coinfection. Immunohistochemistry and in situ hybridization revealed monocytes/macrophages to be the predominant type of cell infiltrating into lung tissues and serving as the major cellular source of chemokines. To explore the causes of chemokine alterations, we treated macaque lung cells with IFN-γ, lipopolysaccharide, Poly(I:C), and P. carinii in vitro, and results revealed that these stimuli can induce the expression of CXCR3 ligand and/or CCR5 ligand mRNAs. Taken together, these studies provide a comprehensive definition of the chemokine networks available to modulate cellular recruitment to lung tissues during SIV infection and implicate both cytokines (IFN-γ) and pathogens (SIV and P. carinii) as contributors to increased expression of pro-inflammatory chemokines.
Ravikumar Muthuswamy, Jan Mueller-Berghaus, Uwe Haberkorn, Todd A. Reinhart, Dirk Schadendorf and Pawel Kalinski
Prostaglandin E2 (PGE2) is an inflammatory mediator often used to increase CCR7 expression in the dendritic cells (DCs) used as cancer vaccines and to enhance their responsiveness to lymph node–associated chemokines. Here, we show that high surface expression of CCR7 on PGE2-matured DCs is associated with their suppressed production of the endogenous CCR7 ligand, CCL19, and is reversible by exogenous CCL19. In contrast to the PGE2-matured DCs, DCs matured in the presence of toll-like receptor (TLR) ligands and interferons produce high levels of both CCL19 and CCR7 mRNA/protein, but show selectively reduced expression of surface CCR7, which is compensated after DC removal from the CCL19-rich maturation environment. In accordance with these findings, PGE2-matured DCs show significantly higher in vitro migratory responsiveness to lymph node–associated chemokines directly after DC generation, but not after additional short-term culture in vitro, nor in vivo in patients injected with 111indium-labeled DCs. The differences in CCL19-producing ability imprinted during DC maturation result in their different abilities to attract CCR7+ naive T cells. Our data help to explain the impact of PGE2 on CCR7 expression in maturing DCs and demonstrate a novel mechanism of regulatory activity of PGE2, mediated by the inhibition of DCs ability to attract naive T cells.