Dr. Jacob Kohlmeier earned his B.S. in Genetics and Ph.D. in Microbiology at the University of Kansas in Lawrence, KS. In the laboratory of Dr. Stephen Benedict, he investigated the role of adhesion molecules on human naïve CD4 T cell function. Jake continued his training as a postdoctoral associate at the Trudeau Institute in Saranac Lake, NY in the laboratory of Dr. David Woodland. There he investigated the generation and recall of cellular immunity to influenza and parainfluenza viruses. Following several years as a research faculty member at Trudeau, Jake accepted a position as an Assistant Professor in the Department of Microbiology and Immunology at Emory University School of Medicine, where he continues to investigate immunity to respiratory pathogens.
The mucosal surfaces of the respiratory, intestinal, and genital tracts are primary portals of entry for a wide range of pathogens. My laboratory studies the generation, maintenance, and recall of cellular immunity in the lung to better understand how pulmonary immune defenses can be harnessed to protect against respiratory pathogens.
The control of influenza and parainfluenza virus infections is mediated in part by T lymphocytes through the production of antiviral cytokines and the lysis of infected host cells within the lung tissue and lung airways. Following resolution of a primary infection, virus-specific memory T cells are established in secondary lymphoid organs and in peripheral tissues such as the lung tissue and lung airways. At the site of pathogen entry in the lung these cells can serve as ‘sentinels’ to alert the immune system should a similar pathogen be reencountered, can help to orchestrate the appropriate secondary immune response, and can limit early pathogen replication.
Using a variety of molecular and genetic approaches to manipulate both the host and the pathogen, we are investigating how lung-resident lymphocytes are programmed to preferentially reside in the different compartments of the lung. We are also investigating the mechanisms these cells use to promote protective immunity, both directly through killing infected cells and indirectly through their interactions with other cells of the innate and adaptive immune system. Our goal is to translate these findings to develop vaccine strategies that promote the most efficacious immune memory for defense against respiratory pathogens. Finally, we are utilizing our knowledge of lung airway immunology during infection to address the dysregulation of immune function in the airways of patients with lung disease, with a particular focus on cystic fibrosis.