Amariliz Rivera
Rutgers University-New Brunswick, NJ·Microbiology & Immunology
Lung infections kill millions of people each year, yet people exposed to the same germ can fare very differently. One reason may be that the lung's frontline immune cells "remember" earlier infections.
- Fields
Microbiology & Immunology
Medicine & Clinical Research
- Topics
trained immunity
innate immunity
alveolar macrophages
- Grants
- 2 known grants, through Jun 2028
What they work on
- Compare how tissue-derived and monocyte-derived alveolar macrophages, two lung immune-cell groups with different origins, reduce pathogen burden and protect lung tissue during helminth, fungal and viral infections, using discovery-based and targeted in vitro and in vivo studies.
- Test whether a previous infection with one pathogen reprograms lung macrophage subsets so that they respond differently to a later, unrelated lung pathogen, a form of innate memory called trained immunity.
- Determine how neutrophil-derived signals and type I and III interferons, which are antiviral signaling proteins, shape the infection-induced responses of TD-AMs and Mo-AMs.
- Investigate how immunization with HK-fbp1, an immunogenic Cryptococcus neoformans strain, primes and trains lung innate immune cells to protect against Aspergillus fumigatus, including under drug-induced immunosuppression.
- Decipher how neutrophils and STAT1-dependent interferon signals guide CCR2+ monocytes as they develop into trained monocyte-derived alveolar macrophages that fight fungi.
More about the research
Macrophages are immune cells that engulf and destroy invaders. Those living in the lung's air sacs are called alveolar macrophages, and they come in two kinds. Tissue-derived alveolar macrophages (TD-AMs) arise from embryonic precursors. Monocyte-derived alveolar macrophages (Mo-AMs) are made later from blood monocytes. The lab's projects ask whether these two kinds do different jobs, and how a past infection reprograms them to respond better to a later, unrelated one. This kind of innate memory is called trained immunity.
Why it matters
Lung infections cause millions of deaths a year, and invasive fungal infections alone kill about 1.5 million people annually, often immunosuppressed patients for whom treatment options are poor. Understanding how lung macrophages are trained by past infections could guide therapies that fine-tune lung inflammation. It could also support vaccines, such as the HK-fbp1 Cryptococcus strain, that protect against several dangerous fungal infections at once.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Lee Quinton
University of Massachusetts Chan Medical School, MA·Microbiology & Immunology
Map when and where CD4+ resident memory T cells, immune cells that stay in previously infected lungs, become activated near airways and veins while neutrophils spread through the lung, using imaging and cytometry in mouse pneumonia.
Christina Leigh Stallings
Washington University in St Louis, MO·Microbiology & Immunology
Define how SPTLC2, the rate-limiting enzyme subunit for building sphingolipids, supports maintenance and monocyte-derived repopulation of alveolar macrophages during M. tuberculosis infection, using mice lacking Sptlc2 in CD11c+ lung cells.
Shelton Wright
University of Washington, WA·Microbiology & Immunology·Early-career
Determine the role of gamma-delta T cells, mucosa-enriched T cells that respond rapidly like innate immune cells, in driving lung inflammation during pulmonary melioidosis in vivo.
The school
Rutgers University-New Brunswick: 57 labs on PI Pages, $837M a year on research, 713 research doctorates a year.
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