About

Amariliz Rivera-Correa, PHD, is an Associate Professor in the Department of Pediatrics at Rutgers New Jersey Medical School and a member of the Center for Immunity and Inflammation. She received her B.S. from the University of Puerto Rico-Mayaguez campus and her PhD from Rutgers-Robert Wood Johnson Medical School. Her postdoctoral training was conducted at Memorial Sloan Kettering Cancer Center under the mentorship of Dr. Eric Pamer, where she focused on understanding how the immune system fights fungal infections. Her research has delineated fungus-specific CD4 T cell responses and innate antifungal immune responses mediated by monocytes, dendritic cells, and neutrophils, particularly in pulmonary fungal disease. Recently, her work uncovered an unexpected role for interferon-γ as a critical instructor of antifungal neutrophil responses via monocyte-derived type I interferon production in the infected lung. Her research is supported by NIAID and the Burroughs Wellcome Fund Investigators in the Pathogenesis of Infectious Disease award, and she has benefited from NIH diversity training initiatives. Her scientific interests include the immune response to fungal pathogens such as Cryptococcus neoformans and Aspergillus fumigatus, focusing on innate and adaptive immunity, T cell differentiation, and the development of vaccines and immunotherapies to combat pulmonary fungal infections.

Research topics

• Immunology
• Biology
• Microbiology
• Cancer research
• Cell biology

Selected publications

• Mannoprotein Cig1 contributes to the immunogenicity of a heat-killed F-box protein Fbp1 <i>Cryptococcus neoformans</i> vaccine model

  Infection and Immunity · 2025-11-28

  articleOpen access

  ABSTRACT Currently, no fungal vaccine exists for clinical use, while fungal infections are responsible for over 1.5 million deaths every year. Our previous studies identified a Cryptococcus neoformans mutant strain fbp1 Δ as a potential vaccine candidate. This strain contains deletion of the F-box protein Fbp1, a key subunit of the SCF E3 ligase complex necessary for ubiquitin-mediated proteolysis. Vaccination with heat-killed fbp1 Δ (HK- fbp1 ) can elicit an interferon gamma (IFN-γ)-dependent Type 1 immune response and provide protection against C. neoformans and its sibling species C. gattii . However, we have yet to decipher the immunogenic factor(s) expressed by the fbp1 ∆ mutant that are responsible for the induction of the protective immune response. In this study, we have identified that the capsule plays an important role in HK- fbp1 vaccine-mediated protection as acapsular HK- fbp1 cells showed diminished protection against wild-type challenge. Additionally, our studies have shown that Cytokine Inducing Glycoprotein 1 (Cig1), a GPI-anchored mannoprotein, is regulated by Fbp1 and contributes to the immunogenicity of HK- fbp1 . Deletion of Cig1 in the fbp1 Δ background resulted in decreased recruitment of antifungal effector T cells and diminished production of protective inflammatory cytokines by the host. Furthermore, loss of Cig1 in the fbp1 Δ mutant resulted in reduced protection in vaccination survival studies at lower vaccine inoculum doses compared to HK- fbp1 . In aggregate, these findings demonstrate Cig1 is an antigen contributing to the immunogenicity of HK- fbp1 that may be utilized to further optimize the HK- fbp1 fungal vaccine as a tool in the arsenal against invasive fungal infections.

  PublisherDOI

• Helminth infection favors reprogramming and proliferation of lung neutrophils

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-03-29

  preprintOpen access

  Neutrophils are a granulocytic population of myeloid cells that have critical effector functions during infectious disease but are generally thought to be short-lived and nonproliferative with markedly limited activation states. In these studies, we directly compared lung neutrophil activation following infection with different groups of pathogens including bacteria, fungi, and helminths. Our results demonstrate considerable heterogeneity depending on the type of infectious agent. In contrast to bacterial and fungal infection, after helminth infection neutrophils expressed markers associated with characteristic type 2 responses and unexpectedly upregulated genes associated with cell cycling and protein synthesis. Further studies showed reduced neutrophil cell death following helminth infection and increased proliferation, which was dependent on IL-4R signaling. This distinct subset of proliferating neutrophils expanded following helminth infection and was released from the endothelial niche to colocalize with invading parasites in the airways. These studies demonstrate a novel long-lived cycling phenotype for neutrophils following helminth infection.

  PublisherOA PDFDOI

• Transient rewilding alters the lung immunologic landscape enhancing host protective responses to helminth infection 3007

  The Journal of Immunology · 2025-11-01

  articleOpen access

  Abstract Description Infection of laboratory-housed mice with the helminth N. brasiliensis (Nb) triggers lung inflammation, contributing to hemorrhaging and acute lung injury (ALI) followed by the development of a polarized type 2 pulmonary immune response and host protective macrophages. (Chen F et al, NI 2014, CR 2022). To examine whether exposure of mice to a rewilding environment might alter this response, mice were housed in an outdoor mesocosm reflecting a natural environment, for five weeks, after which they were returned to the lab and immediately infected with Nb. The RW mice showed a significantly lower worm burden at day 5 after infection. At day 2, increased ALI and lung hemorrhaging, was also significantly reduced.To examine potential changes in the lung immunologic landscape, scRNAseq was performed on rewilded WT and IL-4/IL-13-/- mice. RW WT mice showed significant increases in lung M2 macrophage activation, which was blocked in IL-4/IL-13-/- mice. Inoculation with microbiota isolated from RW mice, which includes Aspergillus species (Yeung F et al, CHM 2020), showed reduced worm burden, hemorrhaging and ALI after Nb infection. Inoculation with RW purified fungi A. fumigatus followed by Nb infection two weeks later showed similar host protective effects. These studies suggest that fungi acquired during transient rewilding can markedly alter pulmonary immune cell activation and function resulting in polarization towards type 2 inflammatory responses. Topic Categories Microbial, Parasitic, and Fungal Immunology (MPF)

  PublisherOA PDFDOI

• Pathogen-tailored role of interferon-λs in neutrophil function during fungal immunity 2235

  The Journal of Immunology · 2025-11-01

  articleOpen accessSenior author

  Abstract Description Aspergillus fumigatus (Af), a ubiquitous airborne fungus, is responsible for more than 90% invasive aspergillosis (IA) cases. Af infections are treated with triazole antifungals. However, these treatments are becoming less effective as Af strains develop resistance. Neutrophils play a crucial role in innate defense against Af. Type I interferons (IFN-I) induce the early production of interferon-lambda (IFN-λ), which controls neutrophil antifungal activity. However, the mechanisms through which IFN-λ modulates neutrophil effector function beyond ROS remain unexplored. We hypothesize that neutrophil-produced IFN-λ is essential for antifungal responses by regulating ISG expression in an autocrine manner. To explore this, we conducted bulk RNA-seq on neutrophils isolated from the lungs of naïve, wild-type (WT), IFNAR-/-, IFNLR-/-, and double knockout (IFNAR-/- IFNLR-/-) mouse models after 48 hours of Aspergillus infection. WT neutrophils exhibited significant upregulation of ISGs, including Oas1, Irf7, Ifit1, Isg15, and Cmpk2, all of which were downregulated in in IFNLR-/- and double knockout cells. We also identified the expression of IFNLR and IFN-λ2/3 in bone marrow neutrophils following Af stimulation. Using phosphoflow, we assess STAT1 activation during neutrophil maturation in response to Af, focusing on STAT1-dependent pathways in IFN-λ-mediated responses. Our findings indicate that IFN-λ is crucial for modulating neutrophil responses to Af via ISGs regulation. Topic Categories Innate Immune Responses and Host Defense: Molecular Mechanisms (INM)

  PublisherOA PDFDOI

• GM-CSF–mediated epithelial-immune cell cross-talk orchestrates pulmonary immunity to Aspergillus fumigatus

  Universität Zürich, ZORA · 2025-03-21

  articleOpen access

  Aspergillus fumigatus causes life-threatening mold pneumonia in immunocompromised patients, particularly in those with quantitative or qualitative defects in neutrophils. Whereas innate immune cell cross-talk licenses neutrophil antifungal activity in the lung, the role of epithelial cells in this process is unknown. Here, we find that surfactant protein C (SPC)–expressing lung epithelial cells integrate infection-induced interleukin-1 and type III interferon signaling to produce granulocyte-macrophage colony-stimulating factor (GM-CSF) preferentially at local sites of fungal infection and neutrophil influx. Using in vivo models that distinguish the role of GM-CSF during acute infection from its homeostatic function in alveolar macrophage survival and surfactant catabolism, we demonstrate that epithelial-derived GM-CSF increases the accumulation and fungicidal activity of GM-CSF–responsive neutrophils, which is essential for host survival. Our findings establish SPC $^{+}$ epithelial cells as a central player in regulating the quality and strength of neutrophil-dependent immunity against inhaled mold pathogens.

  PublisherDOI

• An IFN/STAT1/CYBB axis defines protective plasmacytoid DC–neutrophil crosstalk in Aspergillus fumigatus–infected mice

  Journal of Clinical Investigation · 2025-08-05

  articleOpen access

  Aspergillus fumigatus is the most common cause of invasive aspergillosis (IA), a devastating infection in immunocompromised patients. Plasmacytoid DCs (pDCs) regulate host defense against IA by enhancing neutrophil antifungal properties in the lung. Here, we define the pDC activation trajectory during A. fumigatus infection and the molecular events that underlie the protective pDC-neutrophil crosstalk. Fungus-induced pDC activation began after bone marrow egress and resulted in pDC-dependent regulation of lung type I and type III IFN levels. These pDC-derived products acted on type I and type III IFN receptor-expressing neutrophils and controlled neutrophil fungicidal activity and ROS production via STAT1 signaling in a cell-intrinsic manner. Mechanistically, neutrophil STAT1 signaling regulated transcription and expression of Cybb, which encodes one of 5 NADPH oxidase subunits. Thus, the results indicate that pDCs regulate neutrophil-dependent immunity against inhaled molds by controlling local expression of a subunit required for NADPH oxidase assembly and activity in the lung.

  PublisherOA PDFDOI

• Helminth infection favors persistent and proliferating alternatively activated neutrophils in the lung 2684

  The Journal of Immunology · 2025-11-01

  articleOpen access

  Abstract Description Neutrophils are granulocytic myeloid cells that have critical effector functions during infectious disease but are typically thought to be short-lived, terminally differentiated phagocytic cells. We directly compared lung neutrophil activation following infection with different groups of pathogens including bacteria (Staphylococcus aureus), fungi (Aspergillus fumigatus), and helminths (Nippostrongylus brasiliensis) at 2 days after infection. Our results showed considerable heterogeneity depending on the type of infectious agent. Bulk RNAseq, EdU incorporation, and flow cytometric staining for necrosis/apoptosis identified distinct activation states with rapid cell death predominant in neutrophils after S. aureus and A. fumigatus infection, while neutrophils from helminth infected mice exhibited increased cell cycling and expression of signaling pathways associated with proliferation, type 2 responses, and wound healing. Spectral flow cytometry, intravascular staining, and scRNAseq revealed a distinct c-kit+ proliferating subset of lung neutrophils that expanded shortly after helminth infection and was released from the endothelial niche to co-localize with invading parasites in the airways. These findings challenge current models of neutrophil function during infectious disease, suggesting that neutrophils uniquely assume a persistent and proliferative phenotype that may contribute to tissue repair and resistance in the context of the type 2 pulmonary inflammatory response. Topic Categories Innate Immune Responses and Host Defense: Cellular Mechanisms (INC)

  PublisherOA PDFDOI

• Hide and seek: Cryptococcus evasion of microglial sensing enables meningitis

  Cell Host & Microbe · 2025-12-01

  articleSenior author
  PublisherDOI

• Mycoviruses steer fungal fitness

  Nature Microbiology · 2025-08-22

  articleSenior author
  PublisherDOI

• Mannoprotein Cig1 Contributes to the Immunogenicity of a Heat-Killed F-box Protein Fbp1 <i>Cryptococcus neoformans</i> Vaccine Model

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-06-19

  preprintCorresponding

  Abstract Currently, no fungal vaccine exists for clinical use while fungal infections are responsible for over 1.5 million deaths every year. Our previous studies identified a Cryptococcus neoformans mutant strain fbp1 Δ as a potential vaccine candidate. This mutant strain contains a deletion of the F-box protein Fbp1, a key subunit of the SCF E3 ligase complex necessary for ubiquitin-mediated proteolysis. Vaccination with heat-killed fbp1 Δ (HK- fbp1) can elicit protection against C. neoformans parental strain and its sibling species C. gattii in an interferon gamma (IFN-γ) dependent Type 1 immune response. However, we have yet to decipher the immunogenic factor(s) expressed by the fbp1 Δ mutant that are responsible for the induction of the protective immune response. In this study, we have identified that capsule plays an important role in HK- fbp1 vaccine mediated protection, as acapsular HK- fbp1 cells showed diminished protection against wild type challenge. Additionally, our studies have shown that Cytokine Inducing Glycoprotein 1 (Cig1), a GPI anchored mannoprotein, is regulated by Fbp1 and contributes to the immunogenicity of HK- fbp1 . Deletion of Cig1 in the fbp1 Δ background resulted in decreased recruitment of anti-fungal effector T cells and diminished production of protective inflammatory cytokines by the host. Furthermore, loss of Cig1 in the fbp1 Δ mutant resulted in reduced protection in vaccination survival studies at lower vaccine inoculum doses compared to HK- fbp1 . In aggregate, these findings demonstrate Cig1 is an antigen contributing to the immunogenicity of HK- fbp1 that may be utilized to further optimize the HK- fbp1 fungal vaccine as a tool in the arsenal against invasive fungal infections.

  PublisherDOI

Recent grants

• NIH Grant K01CA117914

  NIH · $637k · 2012

• NIH Grant R21CA167238

  NIH · $375k · 2016

• Regulation of antifungal immunity by monocyte-derived dendritic cells

  NIH · $1.4M · 2015–2021

• Trained immunity and the regulation of anti-fungal defense

  NIH · $3.1M · 2022–2027

• Regulation of antifungal immunity by monocyte-derived dendritic cells

  NIH · $362k · 2015–2020

Frequent coauthors

• Vanessa Espinosa

  Rutgers, The State University of New Jersey

  77 shared

• Tobias M. Hohl

  Memorial Sloan Kettering Cancer Center

  28 shared

• Orchi Dutta

  Rutgers, The State University of New Jersey

  27 shared

• Keyi Wang

  26 shared

• William C. Gause

  Rutgers, The State University of New Jersey

  20 shared

• Alexander Lemenze

  Rutgers New Jersey Medical School

  19 shared

• Mark C. Siracusa

  Rutgers New Jersey Medical School

  19 shared

• Joan E. Durbin

  18 shared

Education

• B.S., Industrial Microbiology

  University of Puerto Rico, Mayaguez

  1993

• Ph.D., Molecular Genetics, Microbiology and Immunology

  UMDNJ-Grauate School of Biomedical Sciences-RWJMS

  2000

Awards & honors

• NCI-CRCHD-Continuing Umbrella of Research Experiences (CURE)
• NIAID research support
• Burroughs Wellcome Fund Investigators in the Pathogenesis of…