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About Us

Invasive fungal infections are a leading cause of death among immunocompromised patients. It is therefore essential to define the cellular and molecular mechanisms of host-pathogen interactions in order to improve outcomes for patients with invasive fungal infections. At the Vyas Laboratory in the Infectious Diseases Division of Massachusetts General Hospital, our research interests lie at the intersection between pathogenic fungal organisms and the immune system.

The first line of defense against these pathogens is phagocytic cells including neutrophils, macrophages, and dendritic cells. Once phagocytes recognize and engulf fungal pathogens, they are placed into membrane-delimited compartments termed phagosomes. In a process known as phagosome maturation, ingested materials are trafficked through a series of increasingly acidified structures, ultimately leading to the degradation of the pathogen. The Vyas Lab uses fungal pathogens of clinical importance including Cryptococcus neoformans, Aspergillus fumigatus and Candida albicans as the model pathogens to study phagosome formation and maturation. Using live cell imaging and fluorescently-tagged proteins, we visualize primary macrophages and their responses to fungi. We examine the role of pattern-recognition receptors such as Dectin-1 and Toll-like receptors in fungal immunity. We are also interested in the role of LC-3 (member of the autophagy family of proteins) and members of the tetraspanin family and their effects on phagosomal maturation. Knowledge gained understanding these molecular events will hopefully tailor the immune response to these clinically relevant fungal pathogens in immunocompromised patients.


View a full list of the Vyas Lab publications on PubMed.

Select Publications


RAW macrophage expressing CD82-RFP (red) and TLR9-GFP (green) simultaneously internalized C. albicans and A. fumigatus conidia. Both CD82 and TLR9 were recruited to the fungal containing phagosomes.
Dendritic cell expressing Class II MHC-GFP (green) sends out tubular projection to Cryptococcus neoformans (red).
A bone marrow derived macrophage co-expresses CD82-RFP (red) and YFP-tubulin (green).
3D cartoon of dendritic cell expressing CD82 (yellow) that has phagocytosed Cryptococcus neoformans (blue).

Principal Investigator

Jatin M. Vyas, MD, PhD
Associate Professor of Medicine, Harvard Medical School
Internal Medicine Residency Program Director, Massachusetts General Hospital
View Dr. Vyas's Harvard Catalyst profile

Lab Members

Jenny M. Tam, PhD
Instructor in Medicine, Harvard Medical School
Assistant in Immunology, Massachusetts General Hospital

Jennifer L. Reedy, MD, PhD
Instructor in Medicine, Harvard Medical School

Allison Timmons, PhD
Medical Writer

Nida S. Khan
Graduate Student

Marianela Feliu
Research Technician II

Paige Negoro
Research Technician

Daniel Lukason
Research Technician

Tammy Vyas
Lab Manager