Amariliz Rivera received her B.S from the University of Puerto Rico-Mayaguez campus and her PhD from Rutgers-Robert
Wood Johnson Medical School. She did her postdoctoral training at MSKCC under the mentorship of Dr. Eric Pamer where
she began the abiding theme of her research-achieving a better understanding of how the immune system fights fungal
infections. After her training, she moved to Rutgers where she is Assistant Professor in the Department of Pediatrics and
member of the Center of Immunity and Inflammation. Her work through the years has delineated fungus-specific CD4 T
cell responses and monocyte-, monocyte-derived dendritic cell- and neutrophil-mediated innate antifungal immune
responses in the context of pulmonary fungal disease. Most recently, her work has uncovered an unexpected of IFN-?s as
critical instructors of antifungal neutrophil responses via monocyte-derived type I interferon production in the infected
lung. Her career has benefited significantly from the NIH efforts to support diversity training and has been the recipient of
multiple awards under the NCI-CRCHD-Continuing Umbrella of Research Experiences (CURE). Her research is currently
supported by NIAID and the Burroughs Wellcome Fund Investigators in the Pathogenesis of Infectious Disease award.
PHD, 2000, UMDNJ-Grauate School of Biomedical Sciences-RWJMS, New Brunswick, NJ, Molecular Genetics, Microbiology and Immunology BS, 1993, University of Puerto Rico, Mayaguez, Puerto Rico, Industrial Microbiology
Masso-Silva J, Espinosa V, Liu T-B, Wang Y, Xue C, Rivera A. 2018. The F box protein 1 Fbp1 shapes the immunogenic
potential of Cryptococcus neoformans. mBio. Jan 9;9(1). pii: e01828-17
Espinosa V. Dutta O, Mc Elrath C, Du P, Chang Y-J, Cicciarelli B, Pitler A, Whitehead I, Obar JJ, Durbin J, Kotenko S.V. and
Rivera A. 2017. Type III interferon is a critical regulator of innate antifungal immunity. Science Immunology. Oct 6;2(16). pii:
Espinosa V, Jhingran A, Dutta O, Kasahara S, Donnelly R, Du P, Rosenfeld R, Leiner I, Chen CC, Ron Y, Hohl TM, Rivera A.
2014. Inflammatory monocytes orchestrate innate antifungal immunity in the lung. PLoS Pathogens. Online publication Feb
Rivera A*, Hohl TM, Collins N, Leiner I, Gallegos A, Saijo S, Coward JW, Iwakura I and Pamer EG. 2011. Dectin-1 diversifies
anti-fungal T cell responses by inhibiting T helper type 1 differentiation. The Journal of Experimental Medicine.
Hohl TM, Rivera A*, Lipuma L, Gallegos A, Shi C, Mack M and Pamer EG. (2009). Pulmonary but not systemic CD4+ T cell
responses require CCR2+Ly6Chi monocyte-derived dendritic cells. Accepted for publication in Cell Host and Microbe 6(5):
Rivera A, Ro G, Van Epps HL, Simpson T, Leiner I, Sant?Angelo DB, Pamer EG. (2006). Innate immune activation and CD4+
T cell priming during respiratory fungal infection. Immunity. 25:665-75.
Areas Of Interest
Innate and Adaptive antifungal immunity
Humans are constantly exposed to a variety of inhaled substances ranging from innocuous particles like pollen and dust to
infectious microorganisms like viruses and fungi. The immune system is thus challenged to trigger protective immune
responses against threatening pathogens while not overreacting to harmless particles. Aspergillus fumigatus is one of the
fungi most commonly present in the environment and it has been estimated that humans can inhale several hundred
spores a day. For the most part exposure to Aspergillus spores does not lead to disease development but patients that lack
a functional immune system due to either genetic deficiencies or as a consequence of immune suppressive therapies can
develop a serious infection (Invasive Aspergillosis, IA). The observation that IA development occurs only in the context of
impaired immunity suggests that the immune system plays a crucial role in preventing infection with this common
environmental fungus. Although fungus-specific immune responses are essential in preventing infection they can also be
detrimental and lead to the development of allergy and asthma. Aspergillus-specific CD4 T cells are central in the
development of allergic airway disease and have been proposed to be an important component of the asthmatic response
in some patients. Our research interests are centered in understanding how innate and adaptive immune responses
coordinate the eradication of A.fumigatus fungal spores while preventing the development of inappropriate responses.
Our research interests are centered in understanding how innate and adaptive
immune responses coordinate the eradication of A.fumigatus fungal spores while preventing the development of
inappropriate responses. In recently published studies our lab uncover a novel role for type III interferons as
critical regulators of the antifungal response of neutrophils in defense against IA. Over the last 5 years my
laboratory has also developed collaborative studies with the Xue lab to uncover host-mediated defense
mechanisms against another clinically relevant fungal pathogen, Cryptococcus neoformans. In studies recently
accepted for publication, our labs determined that the novel virulence factor Fbp1 regulates the immunogenicity
of C. neoformans and demonstrated that a mutant strain lacking Fbp1 serves as an effective vaccine candidate.
In aggregate, our research efforts are centered in developing a better understanding of host-mediated
mechanisms of immune defense against clinically relevant, pulmonary fungal pathogens.