This tool allows searching of HIPC member publications, and provides access to related data when available.
Select one or more filter parameters to filter publications. Don't see a publication ? Access the grant number lookup tool.
reloading
tag filter option
Order tags by
Dataset Availability
Immport Dataset Available (21)
Show all Study ID
SDY1086 (1)
SDY1100 (1)
SDY111 (1)
SDY1119 (1)
SDY112 (4)
SDY113 (2)
SDY1149 (1)
SDY1190 (1)
SDY1230 (5)
SDY1256 (1)
SDY1260 (1)
SDY1264 (1)
SDY1267 (1)
SDY1288 (1)
SDY1324 (1)
SDY1325 (1)
SDY1368 (1)
SDY1369 (1)
SDY1389 (1)
SDY1390 (1)
SDY1393 (1)
SDY1412 (1)
SDY144 (1)
SDY1464 (2)
SDY1465 (2)
SDY1466 (2)
SDY1467 (1)
SDY1468 (1)
SDY1469 (1)
SDY1471 (1)
SDY1472 (1)
SDY1479 (1)
SDY1480 (1)
SDY1481 (1)
SDY1482 (1)
SDY1483 (1)
SDY1484 (1)
SDY1486 (1)
SDY1530 (1)
SDY1538 (1)
SDY1594 (1)
SDY1596 (1)
SDY1600 (2)
SDY162 (1)
SDY1630 (1)
SDY1640 (1)
SDY1654 (1)
SDY1662 (1)
SDY1669 (1)
SDY1708 (1)
SDY1743 (1)
SDY1764 (1)
SDY1767 (1)
SDY1773 (1)
SDY180 (1)
SDY183 (2)
SDY1885 (1)
SDY1968 (1)
SDY1991 (1)
SDY1995 (1)
SDY202 (1)
SDY2044 (1)
SDY207 (1)
SDY212 (6)
SDY215 (1)
SDY2189 (1)
SDY232 (1)
SDY2367 (1)
SDY2617 (1)
SDY2618 (1)
SDY269 (2)
SDY270 (2)
SDY271 (1)
SDY296 (1)
SDY305 (1)
SDY311 (4)
SDY312 (5)
SDY314 (2)
SDY315 (4)
SDY34 (3)
SDY387 (1)
SDY400 (1)
SDY404 (2)
SDY422 (1)
SDY460 (1)
SDY472 (1)
SDY478 (2)
SDY514 (2)
SDY515 (2)
SDY519 (2)
SDY522 (1)
SDY56 (1)
SDY58 (2)
SDY597 (1)
SDY61 (2)
SDY63 (1)
SDY67 (3)
SDY675 (1)
SDY680 (1)
SDY74 (1)
SDY751 (1)
SDY773 (1)
SDY787 (2)
SDY80 (2)
SDY820 (2)
SDY887 (2)
SDY888 (2)
SDY903 (1)
SDY984 (1)
HIPC Centers
Benaroya Research Institute (13)
Columbia University (21)
HIPC 1 (2010) (699)
HIPC 2 (2015) (736)
HIPC 3 (2022) (187)
Icahn School of Medicine at Mount Sinai (31)
La Jolla Institute for Immunology (14)
Massachusetts Institute of technology (14)
Seattle Children's Research Institute (22)
Stanford (51)
Yale University (51)
Publication Keywords
Immport Dataset Available (21)
load all...
show less...
Order publications by
Suryadevara V, Hudgins AD, Rajesh A, Pappalardo A, Karpova A, Dey AK, Hertzel A, Agudelo A, Rocha A, Soygur B, Schilling B, Carver CM, Aguayo-Mazzucato C, Baker DJ, Bernlohr DA, Jurk D, Mangarova DB, Quardokus EM, Enninga EAL, Schmidt EL, Chen F, Duncan FE, Cambuli F, Kaur G, Kuchel GA, ...
Nature reviews. Molecular cell biology
2024-12-01
PMID: 38831121
Animals
Biomarkers
Cellular Senescence
HIPC 1 (2010)
HIPC 2 (2015)
HIPC 3 (2022)
Humans
Mice
Organ Specificity
Yale University
Abstract:
Once considered a tissue culture-specific phenomenon, cellular senescence has now been linked to various biological processes with both beneficial and detrimental roles in humans, rodents and other species. Much of our understanding of senescent cell biology still originates from tissue culture studies, where each cell in the culture is driven to an irreversible cell cycle arrest. By contrast, in tissues, these cells are relatively rare and difficult to characterize, and it is now established that fully differentiated, postmitotic cells can also acquire a senescence phenotype. The SenNet Biomarkers Working Group was formed to provide recommendations for the use of cellular senescence markers to identify and characterize senescent cells in tissues. Here, we provide recommendations for detecting senescent cells in different tissues based on a comprehensive analysis of existing literature reporting senescence markers in 14 tissues in mice and humans. We discuss some of the recent advances in detecting and characterizing cellular senescence, including molecular senescence signatures and morphological features, and the use of circulating markers. We aim for this work to be a valuable resource for both seasoned investigators in senescence-related studies and newcomers to the field.
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.
Wang S, Myers AJ, Irvine EB, Wang C, Maiello P, Rodgers MA, Tomko J, Kracinovsky K, Borish HJ, Chao MC, Mugahid D, Darrah PA, Seder RA, Roederer M, Scanga CA, Lin PL, Alter G, Fortune SM, Flynn JL, Lauffenburger DA
bioRxiv : the preprint server for biology
2024-10-30
PMID: 39554028
HIPC 3 (2022)
Massachusetts Institute of technology
Abstract:
Analysis of multi-modal datasets can identify multi-scale interactions underlying biological systems, but can be beset by spurious connections due to indirect impacts propagating through an unmapped biological network. For example, studies in macaques have shown that BCG vaccination by an intravenous route protects against tuberculosis, correlating with changes across various immune data modes. To eliminate spurious correlations and identify critical immune interactions in a public multi-modal dataset (systems serology, cytokines, cytometry) of vaccinated macaques, we applied Markov Fields (MF), a data-driven approach that explains vaccine efficacy and immune correlations via multivariate network paths, without requiring large numbers of samples (i.e. macaques) relative to multivariate features. Furthermore, we find that integrating multiple data modes with MFs helps to remove spurious connections. Finally, we used the MF to predict outcomes of perturbations at various immune nodes, including a B-cell depletion that induced network-wide shifts without reducing vaccine protection, which we validated experimentally.
Wang S, Myers AJ, Irvine EB, Wang C, Maiello P, Rodgers MA, Tomko J, Kracinovsky K, Borish HJ, Chao MC, Mugahid D, Darrah PA, Seder RA, Roederer M, Scanga CA, Lin PL, Alter G, Fortune SM, Flynn JL, Lauffenburger DA
Cell systems
2024-10-29
PMID: 39504969
HIPC 3 (2022)
Massachusetts Institute of technology
Abstract:
Analysis of multi-modal datasets can identify multi-scale interactions underlying biological systems but can be beset by spurious connections due to indirect impacts propagating through an unmapped biological network. For example, studies in macaques have shown that Bacillus Calmette-Guerin (BCG) vaccination by an intravenous route protects against tuberculosis, correlating with changes across various immune data modes. To eliminate spurious correlations and identify critical immune interactions in a public multi-modal dataset (systems serology, cytokines, and cytometry) of vaccinated macaques, we applied Markov fields (MFs), a data-driven approach that explains vaccine efficacy and immune correlations via multivariate network paths, without requiring large numbers of samples (i.e., macaques) relative to multivariate features. We find that integrating multiple data modes with MFs helps remove spurious connections. Finally, we used the MF to predict outcomes of perturbations at various immune nodes, including an experimentally validated B cell depletion that induced network-wide shifts without reducing vaccine protection.
Davis-Porada J, George AB, Lam N, Caron DP, Gray JI, Huang J, Hwu J, Wells SB, Matsumoto R, Kubota M, Lee Y, Morrison-Colvin R, Jensen IJ, Ural BB, Shaabani N, Weiskopf D, Grifoni A, Sette A, Szabo PA, Teijaro JR, Sims PA, Farber DL
Immunity
2024-10-29
PMID: 39510068
Columbia University
HIPC 2 (2015)
HIPC 3 (2022)
Abstract:
Memory T and B cells in tissues are essential for protective immunity. Here, we performed a comprehensive analysis of the tissue distribution, phenotype, durability, and transcriptional profile of COVID-19 mRNA vaccine-induced immune memory across blood, lymphoid organs, and lungs obtained from 63 vaccinated organ donors aged 23-86, some of whom experienced SARS-CoV-2 infection. Spike (S)-reactive memory T cells were detected in lymphoid organs and lungs and variably expressed tissue-resident markers based on infection history, and S-reactive B cells comprised class-switched memory cells resident in lymphoid organs. Compared with blood, S-reactive tissue memory T cells persisted for longer times post-vaccination and were more prevalent with age. S-reactive T cells displayed site-specific subset compositions and functions: regulatory cell profiles were enriched in tissues, while effector and cytolytic profiles were more abundant in circulation. Our findings reveal functional compartmentalization of vaccine-induced T cell memory where surveilling effectors and in situ regulatory responses confer protection with minimal tissue damage.
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.
Load more...