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HIPC Centers
Benaroya Research Institute (13)
Columbia University (20)
HIPC 1 (2010) (699)
HIPC 2 (2015) (736)
HIPC 3 (2022) (184)
Icahn School of Medicine at Mount Sinai (31)
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Publication Keywords
Immport Dataset Available (21)
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Dalla E, Papanicolaou M, Park MD, Barth N, Hou R, Segura-Villalobos D, Valencia Salazar L, Sun D, Forrest ARR, Casanova-Acebes M, Entenberg D, Merad M, Aguirre-Ghiso JA
Cell
2024-11-14
PMID: 39378878
Animals
Breast Neoplasms
Cell Line, Tumor
Columbia University
Female
HIPC 2 (2015)
HIPC 3 (2022)
Humans
Lung
Lung Neoplasms
Macrophages, Alveolar
Mice
Neoplasm Metastasis
Receptors, Transforming Growth Factor beta
Receptor, Transforming Growth Factor-beta Type II
Signal Transduction
Transforming Growth Factor beta2
Abstract:
Breast disseminated cancer cells (DCCs) can remain dormant in the lungs for extended periods, but the mechanisms limiting their expansion are not well understood. Research indicates that tissue-resident alveolar macrophages suppress breast cancer metastasis in lung alveoli by inducing dormancy. Through ligand-receptor mapping and intravital imaging, it was found that alveolar macrophages express transforming growth factor (TGF)-β2. This expression, along with persistent macrophage-cancer cell interactions via the TGF-βRIII receptor, maintains cancer cells in a dormant state. Depleting alveolar macrophages or losing the TGF-β2 receptor in cancer cells triggers metastatic awakening. Aggressive breast cancer cells are either suppressed by alveolar macrophages or evade this suppression by avoiding interaction and downregulating the TGF-β2 receptor. Restoring TGF-βRIII in aggressive cells reinstates TGF-β2-mediated macrophage growth suppression. Thus, alveolar macrophages act as a metastasis immune barrier, and downregulation of TGF-β2 signaling allows cancer cells to overcome macrophage-mediated growth suppression.
Becker ME, Martin-Sancho L, Simons LM, McRaven MD, Chanda SK, Hultquist JF, Hope TJ
Nature communications
2024-11-02
PMID: 39488529
Bronchi
Cells, Cultured
Cilia
COVID-19
Epithelial Cells
HIPC 2 (2015)
Humans
Mucociliary Clearance
Mucus
Respiratory Mucosa
SARS-CoV-2
Abstract:
SARS-CoV-2 initiates infection in the conducting airways, where mucociliary clearance inhibits pathogen penetration. However, it is unclear how mucociliary clearance impacts SARS-CoV-2 spread after infection is established. To investigate viral spread at this site, we perform live imaging of SARS-CoV-2 infected differentiated primary human bronchial epithelium cultures for up to 12 days. Using a fluorescent reporter virus and markers for cilia and mucus, we longitudinally monitor mucus motion, ciliary motion, and infection. Infected cell numbers peak at 4 days post infection, forming characteristic foci that tracked mucus movement. Inhibition of MCC using physical and genetic perturbations limits foci. Later in infection, mucociliary clearance deteriorates. Increased mucus secretion accompanies ciliary motion defects, but mucociliary clearance and vectorial infection spread resume after mucus removal, suggesting that mucus secretion may mediate MCC deterioration. Our work shows that while MCC can facilitate SARS-CoV-2 spread after initial infection, subsequent MCC decreases inhibit spread, revealing a complex interplay between SARS-CoV-2 and MCC.
de Miguel-Perez D, Arroyo-Hernandez M, La Salvia S, Gunasekaran M, Pickering EM, Avila S, Gebru E, Becerril-Vargas E, Monraz-Perez S, Saharia K, Grazioli A, McCurdy MT, Frieman M, Miorin L, Russo A, Cardona AF, García-Sastre A, Kaushal S, Hirsch FR, Atanackovic D, Sahoo S, Arrieta O, Rolfo C
Journal of extracellular vesicles
2024-11-01
PMID: 39558820
Adult
Aged
Antibodies, Monoclonal, Humanized
Biomarkers
Coronavirus Nucleocapsid Proteins
COVID-19
COVID-19 Drug Treatment
Extracellular Vesicles
Female
HIPC 3 (2022)
Humans
Icahn School of Medicine at Mount Sinai
Interleukin-6
Male
Middle Aged
Multiple Organ Failure
Phosphoproteins
SARS-CoV-2
Severity of Illness Index
Spike Glycoprotein, Coronavirus
Abstract:
The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causes coronavirus disease 2019 (COVID-19) and has been related to more than 7 million deaths globally since 2019. The association of high levels of IL-6 with severe cases led to the early evaluation of the anti-IL6 inhibitor tocilizumab as a potential treatment, which unfortunately failed to improve survival in many trials. Moreover, little is known about the development of COVID-19 sequelae, and biomarkers are needed to understand and anticipate these processes. Because extracellular vesicles (EVs) play an important role in viral infection and immune response, they could potentially serve as predictive and prognostic biomarkers. We isolated EVs from 39 patients with severe COVID-19, from which 29 received tocilizumab and 10 were considered controls. Blood samples, which were collected at hospitalisation before treatment, at Day 7, and Day 15 during follow-up, were assessed by immunoblot for longitudinal expression of spike (S) and nucleocapsid (N) proteins. Dynamic expression was calculated and compared with clinicopathological and experimental variables. Expression of EV S was validated by immunogold and imaging flow-cytometry, revealing an enrichment in CD9+ EVs. As a result, decreasing expression of EV viral proteins was observed in patients treated with tocilizumab. Moreover, higher increase in EV S was observed in patients with lower antibody response, hyperfibrinogenemia, lower respiratory function, higher blood pressure and shorter outcomes. These findings lay the foundation for future studies characterizing the role of EVs in multiorgan assessment and identifying biomarkers in patients with severe COVID-19 and possible long COVID.
Pardi N, Krammer F
Nature reviews. Drug discovery
2024-11-01
PMID: 39367276
Animals
Communicable Diseases
COVID-19
COVID-19 Vaccines
HIPC 3 (2022)
Humans
Icahn School of Medicine at Mount Sinai
mRNA Vaccines
SARS-CoV-2
Vaccine Development
Vaccines, Synthetic
Abstract:
The concept of mRNA-based vaccines emerged more than three decades ago. Groundbreaking discoveries and technological advancements over the past 20 years have resolved the major roadblocks that initially delayed application of this new vaccine modality. The rapid development of nucleoside-modified COVID-19 mRNA vaccines demonstrated that this immunization platform is easy to develop, has an acceptable safety profile and can be produced at a large scale. The flexibility and ease of antigen design have enabled mRNA vaccines to enter development for a wide range of viruses as well as for various bacteria and parasites. However, gaps in our knowledge limit the development of next-generation mRNA vaccines with increased potency and safety. A deeper understanding of the mechanisms of action of mRNA vaccines, application of novel technologies enabling rational antigen design, and innovative vaccine delivery strategies and vaccination regimens will likely yield potent novel vaccines against a wide range of pathogens.
Pallarés HM, González López Ledesma MM, Oviedo-Rouco S, Castellano LA, Costa Navarro GS, Fernández-Alvarez AJ, D'Andreiz MJ, Aldas-Bulos VD, Alvarez DE, Bazzini AA, Gamarnik AV
Nucleic acids research
2024-10-14
PMID: 38917323
Animals
Cell Line
Chlorocebus aethiops
eIF-2 Kinase
HEK293 Cells
HIPC 3 (2022)
Humans
Icahn School of Medicine at Mount Sinai
Protein Biosynthesis
RNA, Untranslated
RNA, Viral
Virus Replication
Zika Virus
Zika Virus Infection
Abstract:
Zika virus (ZIKV) is an emerging mosquito-borne flavivirus that causes severe outbreaks in human populations. ZIKV infection leads to the accumulation of small non-coding viral RNAs (known as sfRNAs) that are crucial for evasion of antiviral responses and for viral pathogenesis. However, the mechanistic understanding of how sfRNAs function remains incomplete. Here, we use recombinant ZIKVs and ribosome profiling of infected human cells to show that sfRNAs block translation of antiviral genes. Mechanistically, we demonstrate that specific RNA structures present in sfRNAs trigger PKR activation, which instead of limiting viral replication, enhances viral particle production. Although ZIKV infection induces mRNA expression of antiviral genes, translation efficiency of type I interferon and interferon stimulated genes were significantly downregulated by PKR activation. Our results reveal a novel viral adaptation mechanism mediated by sfRNAs, where ZIKV increases its fitness by repurposing the antiviral role of PKR into a proviral factor.
Karakus U, Sempere Borau M, Martínez-Barragán P, von Kempis J, Yildiz S, Arroyo-Fernández LM, Pohl MO, Steiger JA, Glas I, Hunziker A, García-Sastre A, Stertz S
Nature microbiology
2024-10-01
PMID: 39009691
Animals
Birds
Cell Line
Chickens
Chiroptera
Ducks
HIPC 3 (2022)
Histocompatibility Antigens Class II
Humans
Icahn School of Medicine at Mount Sinai
Influenza A Virus, H2N2 Subtype
Influenza, Human
Influenza in Birds
N-Acetylneuraminic Acid
Receptors, Virus
Swine
Virus Internalization
Abstract:
Influenza A viruses (IAV) pose substantial burden on human and animal health. Avian, swine and human IAV bind sialic acid on host glycans as receptor, whereas some bat IAV require MHC class II complexes for cell entry. It is unknown how this difference evolved and whether dual receptor specificity is possible. Here we show that human H2N2 IAV and related avian H2N2 possess dual receptor specificity in cell lines and primary human airway cultures. Using sialylation-deficient cells, we reveal that entry via MHC class II is independent of sialic acid. We find that MHC class II from humans, pigs, ducks, swans and chickens but not bats can mediate H2 IAV entry and that this is conserved in Eurasian avian H2. Our results demonstrate that IAV can possess dual receptor specificity for sialic acid and MHC class II, and suggest a role for MHC class II-dependent entry in zoonotic IAV infections.
Kang N, Chawla A, Hillman H, Tippalagama R, Kim C, Mikulski Z, Seumois G, Vijayanand P, Scriba TJ, De Silva AD, Balmaseda A, Harris E, Weiskopf D, Sette A, Arlehamn CL, Peters B, Burel JG
bioRxiv : the preprint server for biology
2024-09-23
PMID: 39386643
HIPC 2 (2015)
HIPC 3 (2022)
La Jolla Institute for Immunology
Abstract:
Communication between immune cells through direct contact is a critical feature of immune responses. Here, we developed a novel high-throughput method to study the transcriptome and adaptive immune receptor repertoire of single cells forming complexes without needing bioinformatic deconvolution. We found that T cells and monocytes forming complexes in blood during active tuberculosis (TB) and dengue hold unique transcriptomic signatures indicative of TCR/MCH-II immune synapses. Additionally, T cells in complexes showed enrichment for effector phenotypes, imaging and transcriptomic features of active TCR signaling, and increased immune activity at diagnosis compared to after anti-TB therapy. We also found evidence for bidirectional RNA exchange between T cells and monocytes, since complexes were markedly enriched for "dual-expressing" cells (i.e., co-expressing T cell and monocyte genes). Thus, studying immune cell complexes at a single-cell resolution offers novel perspectives on immune synaptic interactions occurring in blood during infection.
Holmes EC, Krammer F, Goodrum FD
Cell
2024-09-19
PMID: 39303682
COVID-19
HIPC 3 (2022)
History, 21st Century
Host-Pathogen Interactions
Humans
Icahn School of Medicine at Mount Sinai
Pandemics
SARS-CoV-2
Virology
Virus Diseases
Viruses
Abstract:
Virology has made enormous advances in the last 50 years but has never faced such scrutiny as it does today. Herein, we outline some of the major advances made in virology during this period, particularly in light of the COVID-19 pandemic, and suggest some areas that may be of research importance in the next 50 years. We focus on several linked themes: cataloging the genomic and phenotypic diversity of the virosphere; understanding disease emergence; future directions in viral disease therapies, vaccines, and interventions; host-virus interactions; the role of viruses in chronic diseases; and viruses as tools for cell biology. We highlight the challenges that virology will face moving forward-not just the scientific and technical but also the social and political. Although there are inherent limitations in trying to outline the virology of the future, we hope this article will help inspire the next generation of virologists.
Martino D, Kresoje N, Amenyogbe N, Ben-Othman R, Cai B, Lo M, Idoko O, Odumade OA, Falsafi R, Blimkie TM, An A, Shannon CP, Montante S, Dhillon BK, Diray-Arce J, Ozonoff A, Smolen KK, Brinkman RR, McEnaney K, Angelidou A, Richmond P, Tebbutt SJ, Kampmann B, Levy O, ...
Nature communications
2024-09-17
PMID: 39289350
DNA Methylation
Epigenesis, Genetic
Female
HIPC 2 (2015)
Humans
Infant, Newborn
Lymphocytes
Male
Neutrophils
Polymorphism, Single Nucleotide
Abstract:
Understanding of newborn immune ontogeny in the first week of life will enable age-appropriate strategies for safeguarding vulnerable newborns against infectious diseases. Here we conducted an observational study exploring the immunological profile of infants longitudinally throughout their first week of life. Our Expanded Program on Immunization - Human Immunology Project Consortium (EPIC-HIPC) studies the epigenetic regulation of systemic immunity using small volumes of peripheral blood samples collected from West African neonates on days of life (DOL) 0, 1, 3, and 7. Genome-wide DNA methylation and single nucleotide polymorphism markers are examined alongside matched transcriptomic and flow cytometric data. Integrative analysis reveals that a core network of transcription factors mediates dynamic shifts in neutrophil-to-lymphocyte ratios (NLR), which are underpinned by cell-type specific methylation patterns in the two cell types. Genetic variants are associated with lower NLRs at birth, and healthy newborns with lower NLRs at birth are more likely to subsequently develop sepsis. These findings provide valuable insights into the early-life determinants of immune system development.
Smith D, Eichinger A, Rech A, Wang J, Esteva E, Seyedian A, Yang X, Zhang M, Martinez D, Tan K, Luo M, Park C, Reizis B, Pillai V
bioRxiv : the preprint server for biology
2024-09-09
PMID: 39314418
Columbia University
HIPC 2 (2015)
HIPC 3 (2022)
Abstract:
Castleman disease (CD) is inflammatory lymphoproliferative disorder of unclear etiology. To determine the cellular and molecular basis of CD, we analyzed the spatial proteome of 4,485,009 single cells, transcriptome of 50,117 single nuclei, immune repertoire of 8187 single nuclei, and pathogenic mutations in Unicentric CD, idiopathic Multicentric CD, HHV8-associated MCD, and reactive lymph nodes. CD was characterized by increased non-lymphoid and stromal cells that formed unique microenvironments where they interacted with lymphoid cells. Interaction of activated follicular dendritic cell (FDC) cytoplasmic meshworks with mantle zone B cells was associated with B cell activation and differentiation. VEGF, IL-6, MAPK, and extracellular matrix pathways were elevated in stromal cells of CD. CXCL13+ FDCs, PDGFRA+ T-zone reticular cells (TRC), and ACTA2-positive perivascular reticular cells (PRC) were identified as the predominant source of increased VEGF expression and IL-6 signaling in CD. VEGF expression by FDCs was associated with peri-follicular neovascularization. FDC, TRC and PRC of CD activated JAK-STAT, TGFβ, and MAPK pathways via ligand-receptor interactions involving collagen, integrins, complement components, and VEGF receptors. T, B and plasma cells were polyclonal but showed class-switched and somatically hypermutated IgG1+ plasma cells consistent with stromal cell-driven germinal center activation. In conclusion, our findings show that stromal cell activation and associated B-cell activation and differentiation, neovascularization and stromal remodeling underlie CD and suggest new targets for treatment.
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