Melanie Harriff, Ph.D.
- Associate Professor of Medicine, Division of Pulmonary and Critical Care Medicine, School of Medicine
Biography
Melanie Harriff received her Ph.D. in Molecular and Cellular Biology in 2007 from Oregon State University in the laboratories of Luiz Bermudez and Michael Kent. Following a year-long postdoctoral research position in the laboratory of Gary Thomas at the Vollum Institute at Oregon Health & Sciences University, Harriff worked as a postdoctoral research fellow in the Department of Pulmonary and Critical Care Medicine at OHSU, in the laboratory of David Lewinsohn. She joined the Research Department at the Portland VA Medical Center as a Research Microbiologist in 2011, and is also an Associate Professor in the Department of Pulmonary and Critical Care Medicine at OHSU.
Education and training
-
Degrees
- Ph.D., 2007, Oregon State University
-
Fellowship
- Postdoctoral Fellowship, Oregon Health & Science University, 2011
Publications
Publications
Delivery of loaded MR1 monomer results in efficient ligand exchange to host MR1 and subsequent MR1T cell activation
Communications BiologyChronic Obstructive Pulmonary Disease and Cigarette Smoke Lead to Dysregulated Mucosal-associated Invariant T-Cell Activation
American journal of respiratory cell and molecular biologyPhagocytosis is a primary determinant of pulmonary clearance of clinical Klebsiella pneumoniae isolates
Frontiers in Cellular and Infection MicrobiologyAugmentation of the Riboflavin-Biosynthetic Pathway Enhances Mucosa-Associated Invariant T (MAIT) Cell Activation and Diminishes Mycobacterium tuberculosis Virulence
mBioDeaza-modification of MR1 ligands modulates recognition by MR1-restricted T cells
Scientific ReportsConstruction and validation of an ultraviolet germicidal irradiation system using locally available components
PloS oneAlternative splicing of MR1 regulates antigen presentation to MAIT cells
Scientific ReportsRab6 regulates recycling and retrograde trafficking of MR1 molecules
Scientific ReportsMR1 recycling and blockade of endosomal trafficking reveal distinguishable antigen presentation pathways between Mycobacterium tuberculosis infection and exogenously delivered antigens
Scientific ReportsMAIT cells and microbial immunity
Immunology and Cell BiologyMR1 displays the microbial metabolome driving selective MR1-restricted T cell receptor usage
Science ImmunologyRiboflavin metabolism variation among clinical isolates of streptococcus pneumoniae results in differential activation of mucosal-Associated invariant T cells
American journal of respiratory cell and molecular biologyRole of MAIT cells in pulmonary bacterial infection
Molecular ImmunologyHLA-E Presents Glycopeptides from the Mycobacterium tuberculosis Protein MPT32 to Human CD8+ T cells
Scientific ReportsMR1-restricted mucosal-associated invariant T (MAIT) cells respond to mycobacterial vaccination and infection in nonhuman primates
Mucosal ImmunologyT cell recognition of Mycobacterium tuberculosis peptides presented by HLA-E derived from infected human cells
PloS oneThe Mycobacterium tuberculosis MmpL11 cell wall lipid transporter is important for biofilm formation, intracellular growth, and nonreplicating persistence
Infection and ImmunityEndosomal MR1 Trafficking Plays a Key Role in Presentation of Mycobacterium tuberculosis Ligands to MAIT Cells
PLoS pathogensHuman TRAV1-2-negative MR1-restricted T cells detect S. pyogenes and alternatives to MAIT riboflavin-based antigens
Nature communicationsHuman lung epithelial cells contain Mycobacterium tuberculosis in a late endosomal vacuole and are efficiently recognized by CD8+ T Cells
PloS oneTAP mediates import of Mycobacterium tuberculosis-derived peptides into phagosomes and facilitates loading onto HLA-I
PloS oneHuman mucosal associated invariant T cells detect bacterially infected cells
PLoS BiologyMycobacterium avium genes MAV-5138 and MAV-3679 are transcriptional regulators that play a role in invasion of epithelial cells, in part by their regulation of CipA, a putative surface protein interacting with host cell signaling pathways
Journal of bacteriologyThe Mycobacterium tuberculosis Phagosome Is a HLA-I Processing Competent Organelle
PLoS pathogens