Sing Sing Way, MD, PhD

My Biography & Research My Education My Publications

Pauline and Lawson Reed Chair, Division of Infectious Diseases

Associate Professor, UC Department of Pediatrics

My Biography & Research

Biography

Dr. Way is an infectious disease physician-scientist. He cares for infants and children with infection related illness, and provides consultation in the diagnosis and prevention diseases caused by communicable agents. Dr. Way supervises an active basic research laboratory that uses basic immunological approaches to investigate ways to boost host defense and protection against infection. Ongoing projects investigate the immune basis responsible for enhanced susceptibility to infection during pregnancy, the immune pathogenesis of pregnancy complications that occur with maternal infection, and the basic signals required for stimulating immune cell activation.

Dr. Way trained in the combined MD/PhD program at the Albert Einstein College of Medicine, pediatric residency at the University of California San Francisco, and infectious disease fellowship at the University of Washington. During fellowship training, Dr. Way began investigating the basic immunology and immune pathogenesis of infectious diseases relevant to human, and in particular, infant and child health.

Dr. Way’s research has been supported by the National Institutes of Health since 2006. Dr. Way’s research has been described in many publications in numerous prestigious scientific journals including Nature, Cell Host & Microbe, PLoS Pathogens, and The Journal of Immunology. The past and ongoing work has also been recognized by numerous prestigious awards including the Infectious Diseases Society of America Wyeth Young Investigator Award, a Basil O’ Conner Award from the March of Dimes Foundation, and the Investigator in Pathogenesis of Infectious Diseases award from the Burroughs Wellcome Fund.

Academic Affiliation

Associate Professor, UC Department of Pediatrics

Departments

Infectious Diseases, Infectious Diseases, Center for Prevention of Preterm Birth, Center for Inflammation and Tolerance

My Education

MD PhD: Albert Einstein College of Medicine, Bronx, NY, 1999.

Residency: University of California San Francisco, San Francisco, CA, 2001.

Fellowship: University of Washington, Seattle, WA, 2004.

My Publications

Rowe JH, Ertelt JM, Xin L, Way SS. Pregnancy imprints regulatory memory that sustains anergy to fetal antigen. Nature. 490: 102-106. 2012.

Rowe JH, Ertelt JM, Xin L, Way SS. Listeria monocytogenes cytoplasmic entry induces fetal wastage by disrupting maternal Foxp3+ regulatory T cell-sustained fetal tolerance. PLoS Pathog. 8: e1002873. 2012.

Rowe JH, Ertelt JM, Way SS. Innate IFN-g is essential for Programmed death ligand-1-mediated T cell stimulation following Listeria monocytogenes infection. J Immunol. 189: 876-84. 2012.

Rowe JH, Ertelt JM, Way SS. Foxp3+ regulatory T cells, immune stimulation, and host defense against infection. Immunology. 136:1-10. 2011.

Ertelt JM, Johanns TM, Mysz MA, Nanton MR, Rowe JH, Aguilera MN, Way SS. Selective culling of high avidity antigen-specific CD4+ T cells after virulent Salmonella infection. Immunology. 134: 487-97. 2011.

Ertelt JM, Rowe JH, Mysz MA, Singh C, Roychowdhury M, Aguilera MN, Way SS. Foxp3+ regulatory T cells impede the priming of protective CD8+ T cells. J Immunol. 187: 2569-77. 2011.

Rowe JH, Ertelt JM, Aguilera MN, Farrar MA, Way SS. Foxp3+ regulatory T cell expansion required for sustaining pregnancy compromises host defense against prenatal bacterial pathogens. Cell Host Microbe. 10:54-64. 2011.

Johanns TM, Law CY, Kalekar LA, O’Donnell H, Ertelt JM, Rowe JH, Way SS. Early eradication of persistent Salmonella infection primes antibody-mediated protective immunity to recurrent infection. Microbes Infect. 13: 322-330. 2011.

Han JY, Hanson DC, Way SS. Herpes Zoster and meningitis due to reactivation of varicella vaccine virus in a immunocompetent child. Pediatr Infect Dis J. 30:266-268. 2011.

Ertelt JM, Johanns TM, Rowe JH, Way SS. IL-21-independent pathogen-specific CD8+ T cell expansion, and IL-21-dependnent suppression of CD4+ T cell IL-17 production. Immunology. 131: 183-191. 2010.