Dr. Carpenter received his MD and PhD degrees from the University of Massachusetts (UMass) Medical School (Worcester, MA), completed an Internal Medicine residency at the NYU School of Medicine (New York, NY), and a Fellowship in Infectious Diseases at Harvard Medical School / Massachusetts General Hospital / Brigham and Women’s Hospital (Boston, MA). Carpenter received his scientific training in the lab of Dr. Sam Behar at Brigham and Women’s Hospital (2011-2013) and at UMass Medical School (2013 - 2017) where he served as Instructor of Microbiology and Physiological Systems. In Dr. Behar’s lab he studied vaccine-elicited memory T cell responses to Mycobacterium tuberculosis (Mtb) in the mouse model of tuberculosis (TB). Dr. Carpenter also served as Attending Physician on the Transplant and Immunocompromised Host Infectious Disease consult service at the Brigham and Women’s Hospital and Dana Farber Cancer Institute (2012 - 2017). In 2017, Dr. Carpenter was recruited to Regeneron Pharmaceuticals where he served as Director of Early Clinical Development and Experimental Sciences and received clinical and translational research training, focusing on programs in transplant immunology and infectious diseases in the immunocompromised host. In 2020, Dr. Carpenter was recruited to the Division of Infectious Diseases and HIV Medicine at ÐÇ¿Õ´«Ã½ / University Hospitals Cleveland Medical Center as Assistant Professor of Medicine in the tenure track. Dr. Carpenter’s lab studies human T cell and macrophage responses to Mycobacterium tuberculosis and other chronic infectious diseases.
My lab focuses on how human T cells and macrophages interact and respond during early infection with Mycobacterium tuberculosis (Mtb). We use fluorescence-activated cell sorting (FACS) of human memory T cells from individuals with latent Mtb infection (LTBI) to identify CD4+ T cells that recognize Mtb-infected macrophages, followed by single-cell transcriptomics, surface receptor profiling, and T cell antigen receptor (TCR) sequencing. This platform allows us to compare the functions of individual TCR clonotypes in response to Mtb-infected macrophages to define T cell functions and antigen specificities that can inform the design of protective TB vaccines.