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Benaroya Research Institute (13)
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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
2024-12-18
PMID: 39504969
Administration, Intravenous
Animals
BCG Vaccine
B-Lymphocytes
HIPC 3 (2022)
Immune System
Macaca
Macaca mulatta
Markov Chains
Massachusetts Institute of technology
Tuberculosis
Vaccination
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.
Dib SM, Wimalasena S, Graciaa DS, Rouphael N
The Journal of infectious diseases
2024-12-16
PMID: 39424292
HIPC 3 (2022)
Humans
Precision Medicine
Stanford
Systems Biology
Vaccination
Vaccines
Vaccine Development
Vaccinology
Abstract:
Systems vaccinology integrates a range of "omics" technologies to identify key immune signatures and enhance vaccine development. This approach aids in understanding variations in immune responses, driven by genetics, health status, and the microbiome. Consequently, systems vaccinology helps pave the way for personalized vaccination strategies, essential for addressing diverse populations.
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
2024-12-10
PMID: 39510068
Adult
Aged
Aged, 80 and over
B-Lymphocytes
Columbia University
COVID-19
COVID-19 Vaccines
Female
HIPC 2 (2015)
HIPC 3 (2022)
Humans
Immunologic Memory
Lung
Lymphoid Tissue
Male
Memory T Cells
Middle Aged
SARS-CoV-2
Spike Glycoprotein, Coronavirus
Vaccination
Young Adult
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.
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.
Maguire C, Chen J, Rouphael N, Pickering H, Phan HV, Glascock A, Chu V, Dandekar R, Corry D, Kheradmand F, Baden LR, Selaky R, McComsey GA, Haddad EK, Cairns CB, Pulendran B, Fernandez-Sesma A, Simon V, Metcalf JP, Higuita NIA, Messer WB, David MM, Nadeau KC, Kraft M, Bime C, ...
bioRxiv : the preprint server for biology
2024-11-16
PMID: 39605478
HIPC 1 (2010)
HIPC 2 (2015)
HIPC 3 (2022)
Yale University
Abstract:
Chronic viral infections are ubiquitous in humans, with individuals harboring multiple latent viruses that can reactivate during acute illnesses. Recent studies have suggested that SARS-CoV-2 infection can lead to reactivation of latent viruses such as Epstein-Barr Virus (EBV) and cytomegalovirus (CMV), yet, the extent and impact of viral reactivation in COVID-19 and its effect on the host immune system remain incompletely understood. Here we present a comprehensive multi-omic analysis of viral reactivation of all known chronically infecting viruses in 1,154 hospitalized COVID-19 patients, from the Immunophenotyping Assessment in a COVID-19 Cohort (IMPACC) study, who were followed prospectively for twelve months. We reveal significant reactivation of Herpesviridae, Enteroviridae, and Anelloviridae families during acute stage of COVID-19 (0-40 days post-hospitalization), each exhibiting distinct temporal dynamics. We also show that viral reactivation correlated with COVID-19 severity, demographic characteristics, and clinical outcomes, including mortality. Integration of cytokine profiling, cellular immunophenotyping, metabolomics, transcriptomics, and proteomics demonstrated virus-specific host responses, including elevated pro-inflammatory cytokines (e.g. IL-6, CXCL10, and TNF), increased activated CD4+ and CD8+ T-cells, and upregulation of cellular replication genes, independent of COVID-19 severity and SARS-CoV-2 viral load. Notably, persistent Anelloviridae reactivation during convalescence (≥3 months post-hospitalization) was associated with Post-Acute Sequelae of COVID-19 (PASC) symptoms, particularly physical function and fatigue. Our findings highlight a remarkable prevalence and potential impact of chronic viral reactivation on host responses and clinical outcomes during acute COVID-19 and long term PASC sequelae. Our data provide novel immune, transcriptomic, and metabolomic biomarkers of viral reactivation that may inform novel approaches to prognosticate, prevent, or treat acute COVID-19 and PASC.
Moore AR, Zheng H, Ganesan A, Hasin-Brumshtein Y, Maddali MV, Levitt JE, van der Poll T, Scicluna BP, Giamarellos-Bourboulis EJ, Kotsaki A, Martin-Loeches I, Garduno A, Rothman RE, Sevransky J, Wright DW, Atreya MR, Moldawer LL, Efron PA, Marcela K, Karvunidis T, Giannini HM, Meyer NJ, Sweeney TE, Rogers AJ, Khatri P
bioRxiv : the preprint server for biology
2024-11-15
PMID: 39605502
HIPC 3 (2022)
Stanford
Abstract:
Progress in the management of critical care syndromes such as sepsis, Acute Respiratory Distress Syndrome (ARDS), and trauma has slowed over the last two decades, limited by the inherent heterogeneity within syndromic illnesses. Numerous immune endotypes have been proposed in sepsis and critical care, however the overlap of the endotypes is unclear, limiting clinical translation. The SUBSPACE consortium is an international consortium that aims to advance precision medicine through the sharing of transcriptomic data. By evaluating the overlap of existing immune endotypes in sepsis across over 6,000 samples, we developed cell-type specific signatures to quantify dysregulation in these immune compartments. Myeloid and lymphoid dysregulation were associated with disease severity and mortality across all cohorts. This dysregulation was not only observed in sepsis but also in ARDS, trauma, and burn patients, indicating a conserved mechanism across various critical illness syndromes. Moreover, analysis of randomized controlled trial data revealed that myeloid and lymphoid dysregulation is linked to differential mortality in patients treated with anakinra or corticosteroids, underscoring its prognostic and therapeutic significance. In conclusion, this novel immunology-based framework for quantifying cellular compartment dysregulation offers a valuable tool for prognosis and therapeutic decision-making in critical illness.
Brook B, Checkervarty AK, Barman S, Sweitzer C, Bosco AN, Sherman AC, Baden LR, Morrocchi E, Sanchez-Schmitz G, Palma P, Nanishi E, O'Meara TR, McGrath ME, Frieman MB, Soni D, van Haren SD, Ozonoff A, Diray-Arce J, Steen H, Dowling DJ, Levy O
iScience
2024-11-15
PMID: 39569372
HIPC 2 (2015)
Abstract:
mRNA vaccines demonstrate impaired immunogenicity and durability in vulnerable older populations. We hypothesized that human in vitro modeling and proteomics could elucidate age-specific mRNA vaccine actions. BNT162b2-stimulation changed the plasma proteome of blood samples from young (18-50Y) and older adult (≥60Y) participants, assessed by mass spectrometry, proximity extension assay, and multiplex. Young adult up-regulation (e.g., PSMC6, CPN1) contrasted reduced induction in older adults (e.g., TPM4, APOF, APOC2, CPN1, PI16). 30-85% lower TH1-polarizing cytokines and chemokines were induced in elderly blood (e.g., IFNγ, CXCL10). Analytes lower in older adult samples included human in vivo mRNA immunogenicity biomarkers (e.g., IFNγ, CXCL10, CCL4, IL-1RA). BNT162b2 also demonstrated reduced CD4+ TH1 responses in aged vs. young adult mice. Our study demonstrates the utility of human in vitro platforms modeling age-specific mRNA vaccine immunogenicity, highlights impaired support of TH1 polarization in older adults, and provides a rationale for precision mRNA vaccine adjuvantation to induce greater immunogenicity.
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.
Jasset OJ, Lopez Zapana PA, Bahadir Z, Shook L, Dennis M, Gilbert E, Liu ZA, Yinger RV, Bald C, Bradford CG, Silfen AH, Klein SL, Pekosz A, Permar S, Konnikova L, Yonker LM, Lauffenburger D, Nelson A, Elovitz MA, Edlow AG
American journal of obstetrics and gynecology
2024-11-07
PMID: 39515450
HIPC 3 (2022)
Massachusetts Institute of technology
Abstract:
[{'@Label': 'BACKGROUND', '@NlmCategory': 'BACKGROUND', '#text': 'Respiratory syncytial virus is associated with significant neonatal and infant morbidity and mortality. Maternal bivalent respiratory syncytial virus prefusion F respiratory syncytial virus vaccination to protect neonates and infants was approved in September 2023 for administration between 32+0 and 36+6\xa0weeks to protect neonates and infants. This approved timeframe is narrower than the 24 to 36\xa0week window evaluated in the clinical trial, due to the possible association between preterm birth and vaccine administration. Currently, data are lacking on how maternal vaccine timing within the approved window affects the transfer of antibodies from mother to fetus, critical information that could influence clinical practice.'}, {'@Label': 'OBJECTIVE', '@NlmCategory': 'OBJECTIVE', '#text': 'We sought to examine how gestational age at vaccination and time elapsed from maternal respiratory syncytial virus vaccination to delivery impacted transfer of maternal antibodies measured in the umbilical cord at delivery and in peripheral blood of 2-month infants. We also examined differences in maternal and cord respiratory syncytial virus antibody levels achieved by vaccination vs natural RSV infection.'}, {'@Label': 'STUDY DESIGN', '@NlmCategory': 'METHODS', '#text': 'A prospective cohort study was conducted at 2 academic medical centers between September 20, 2023 and March 21, 2024, enrolling 124 individuals who received the respiratory syncytial virus vaccine during pregnancy. Infant capillary blood was collected at 2\xa0months of age from 29 of the infants. Maternal and cord immunoglobulin G levels achieved by respiratory syncytial virus vaccination were compared to those associated with maternal natural respiratory syncytial virus infection, using banked blood from 20 maternal:cord dyads collected prior to the availability of the maternal respiratory syncytial virus vaccine. Levels of immunoglobulin G against respiratory syncytial virus strain A2 and B fusion (F) and attachment (G) proteins and against pertussis toxin (as a comparator antigen from a vaccine routinely administered earlier in pregnancy) were measured using a Binding Antibody Multiplex Assay. Differences in titers between vaccination and natural infection were examined using Wilcoxon rank-sum test. Differences in cord:maternal transfer ratios and 2-month infant antibody levels by timing of maternal vaccination were evaluated by Kruskal-Wallis testing.'}, {'@Label': 'RESULTS', '@NlmCategory': 'RESULTS', '#text': 'Maternal respiratory syncytial virus vaccination resulted in significantly higher maternal and cord antirespiratory syncytial virus F antibody levels than natural infection (5.72 vs 4.82 log10 mean fluorescence intensity, P<.0001 maternal; 5.81 vs 5.03 log10 mean fluorescence intensity, P<.0001 cord). Maternal vaccination 2 to 3\xa0weeks and 3 to 4\xa0weeks prior to delivery was associated with significantly lower cord:maternal transfer ratios than were observed when vaccination occurred >5\xa0weeks prior to delivery (P=.03 for 2-3\xa0weeks, P=.007 for 3-4\xa0weeks), and significantly lower transfer ratios than observed for pertussis vaccination administered prior to 30\xa0weeks of gestation (P=.008 for 2-3\xa0weeks, P=.03 for 3-4\xa0weeks, similar at >4\xa0weeks).'}, {'@Label': 'CONCLUSION', '@NlmCategory': 'CONCLUSIONS', '#text': 'Vaccine administration earlier in the approved 32 to 36\xa0week window (at least 5\xa0weeks prior to delivery) results in the highest transplacental transfer of maternal antibodies to the neonate. These results should inform the counseling of pregnant individuals on optimal vaccination timing.'}]
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.
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