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 (140)
Show all Study ID
SDY1041 (1)
SDY1086 (1)
SDY1092 (1)
SDY1097 (1)
SDY1100 (1)
SDY1108 (1)
SDY1109 (1)
SDY111 (1)
SDY1119 (1)
SDY112 (4)
SDY113 (2)
SDY1149 (1)
SDY1190 (1)
SDY1230 (6)
SDY1256 (1)
SDY1260 (1)
SDY1264 (1)
SDY1267 (2)
SDY1276 (2)
SDY1288 (1)
SDY1289 (1)
SDY1291 (1)
SDY1293 (1)
SDY1294 (1)
SDY1324 (1)
SDY1325 (1)
SDY1328 (1)
SDY1361 (1)
SDY1364 (2)
SDY1368 (1)
SDY1369 (1)
SDY1373 (1)
SDY1385 (1)
SDY1389 (1)
SDY1390 (1)
SDY1393 (1)
SDY1412 (1)
SDY1439 (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)
SDY1641 (1)
SDY1648 (1)
SDY1654 (1)
SDY1655 (1)
SDY1662 (1)
SDY1669 (1)
SDY167 (1)
SDY1708 (1)
SDY1743 (1)
SDY1764 (1)
SDY1767 (1)
SDY1773 (1)
SDY180 (1)
SDY183 (2)
SDY1885 (1)
SDY1886 (1)
SDY1968 (1)
SDY1991 (1)
SDY1995 (1)
SDY202 (1)
SDY207 (1)
SDY212 (6)
SDY215 (1)
SDY2165 (1)
SDY2188 (1)
SDY2189 (1)
SDY224 (2)
SDY232 (2)
SDY2367 (1)
SDY241 (6)
SDY2429 (1)
SDY2617 (1)
SDY2618 (1)
SDY269 (2)
SDY270 (2)
SDY271 (1)
SDY28 (5)
SDY2917 (1)
SDY2948 (1)
SDY296 (1)
SDY299 (4)
SDY305 (1)
SDY311 (4)
SDY312 (5)
SDY314 (2)
SDY315 (4)
SDY34 (3)
SDY387 (1)
SDY400 (2)
SDY404 (3)
SDY422 (1)
SDY460 (1)
SDY472 (1)
SDY478 (2)
SDY514 (2)
SDY515 (2)
SDY519 (2)
SDY520 (1)
SDY522 (1)
SDY56 (1)
SDY58 (2)
SDY597 (1)
SDY61 (2)
SDY614 (2)
SDY63 (2)
SDY67 (4)
SDY675 (1)
SDY680 (1)
SDY690 (4)
SDY702 (1)
SDY74 (1)
SDY751 (1)
SDY773 (1)
SDY787 (2)
SDY789 (1)
SDY80 (2)
SDY816 (4)
SDY820 (2)
SDY887 (2)
SDY888 (2)
SDY89 (4)
SDY903 (1)
SDY984 (1)
HIPC Centers
Benaroya Research Institute (13)
Columbia University (28)
HIPC 1 (2010) (712)
HIPC 2 (2015) (767)
HIPC 3 (2022) (231)
Icahn School of Medicine at Mount Sinai (33)
La Jolla Institute for Immunology (16)
Massachusetts Institute of technology (17)
Seattle Children's Research Institute (25)
Stanford (73)
Yale University (61)
Publication Keywords
Immport Dataset Available (140)
load all...
show less...
Order publications by
Kollmann TR, Amenyogbe N, Schaltz-Buchholzer F, Bæk O, Campbell J, Lynn DJ, Campbell AJ, Aaby P, Stabell Benn C, Netea MG, Divangahi M
The Journal of infectious diseases
2025-07-11
PMID: 39913242
Animals
Bacteremia
BCG Vaccine
HIPC 2 (2015)
Humans
Infant, Newborn
Mycobacterium tuberculosis
Tuberculosis
Vaccination
Abstract:
Tuberculosis (TB) is caused by Mycobacterium tuberculosis (Mtb) and is a leading cause of death. BCG is the only licensed TB vaccine. Preclinical studies have shown that in adults, intravenous administration of BCG improves protection against TB. We hypothesize that intradermal administration of BCG to the human newborn leads to low-grade BCG bacteremia and that this systemic dissemination improves protection against Mtb infection. This hypothesis is based on supporting observations including animal and human studies. It is a testable hypothesis and offers to deliver immediately actionable insight to advance the global efforts against TB.
Smith D, Eichinger A, Fennell É, Xu-Monette ZY, Rech A, Wang J, Esteva E, Seyedian A, Yang X, Zhang M, Martinez D, Tan K, Luo M, Young KJ, Murray PG, Park C, Reizis B, Pillai V
Nature communications
2025-07-01
PMID: 40593805
Adult
Aged
B-Lymphocytes
Castleman Disease
Cell Differentiation
Chemokine CXCL13
Columbia University
Cytokines
Dendritic Cells, Follicular
Female
HIPC 2 (2015)
HIPC 3 (2022)
Humans
Interleukin-6
Lymph Nodes
Lymphocyte Activation
Male
Middle Aged
Signal Transduction
Single-Cell Analysis
Stromal Cells
Transcriptome
Vascular Endothelial Growth Factor A
Abstract:
To determine the cellular and molecular basis of Castleman Disease (CD), we analyze the spatial proteome and transcriptome from a discovery (n = 9 cases) and validation (n = 13 cases) cohort of Unicentric CD, idiopathic Multicentric CD, HHV8-associated MCD, and reactive lymph nodes. CD shows increased stromal cells that form unique microenvironments. Interaction of activated follicular dendritic cell (FDC) cytoplasmic meshworks with mantle-zone B cells is associated with B-cell activation and differentiation. CXCL13+ FDCs, PDGFRA + T-zone reticular cells (TRC), and ACTA2-positive perivascular reticular cells (PRC) were the predominant source of increased VEGF expression and IL-6 signaling. MCD is characterized by increased TRC while UCD shows increased B-reticular cells (BRC). VEGF expression by FDCs is associated with peri-follicular neovascularization. FDC, TRC and PRC of CD activates JAK-STAT, TGFβ, and MAPK pathways via specific ligand-receptor interactions. Here, we show that stromal-cell activation and associated B cell activation and differentiation, neovascularization and stromal remodeling underlie CD.
Tsai W-Y, Tseng AC, Chen G-H, Hsieh S-C, Balmaseda A, Nerurkar VR, Harris E, Wang W-K
Microbiology spectrum
2025-07-01
PMID: 40401969
Antibodies, Viral
Child
Child, Preschool
Female
HIPC 2 (2015)
Humans
Infant
Male
Nicaragua
Viral Envelope Proteins
West Nile Fever
West Nile virus
Zika Virus
Zika Virus Infection
Abstract:
[{'@Label': 'UNLABELLED', '#text': 'Since its introduction to the Western Hemisphere in 1999 in New York City, West Nile virus (WNV) has spread throughout the continental USA and moved into Canada, Mexico, Caribbean, and Central and South Americas. While WNV has caused ~7 million human infections and >59,000 cases in the USA and >6,000 cases in Canada, only few human cases have been reported in Latin America. Due to the cross-reactivity of anti-envelope antibodies, the detection of WNV infection by serology to explore its epidemiology in Latin America, where multiple flaviviruses co-circulate, remains a challenge. Previously, we reported that anti-premembrane (prM) antibodies can distinguish between four flavivirus (WNV, dengue, Zika, and yellow fever viruses) infections. In this study, we examined 73 samples from 40 Zika cases from a pediatric cohort in Nicaragua using Western blot analysis and detected anti-prM antibodies to WNV in three participants in samples collected between 2016 and 2017, suggesting previous WNV infection prior to ZIKV infection. Analysis of available archived samples revealed anti-WNV prM antibodies in the earliest samples (2007-2009), which were further confirmed by plaque reduction neutralization test, suggesting that they were infected by WNV prior to 2007-2009. Our report of WNV infection in three Nicaraguan children, corresponding to a seropositive rate of 7.5%, highlights the transmission of WNV in humans in Central America prior to 2007. Future studies with improved serological tests for WNV surveillance in Latin America are needed to enhance our understanding of the epidemiology and transmission of WNV in the Western Hemisphere.'}, {'@Label': 'IMPORTANCE', '@NlmCategory': 'OBJECTIVE', '#text': 'Since its arrival to North America in 1999, West Nile virus (WNV) has caused multiple outbreaks in birds and humans, with thousands of human cases in the USA and Canada, whereas in Latin America, WNV has mainly been detected in birds and horses with few human cases. Due to cross-reactivity of anti-envelope antibodies among different flaviviruses, detection of WNV infection by serology to explore its epidemiology in Latin America remains a challenge. Previously, we reported that anti-premembrane antibodies can discriminate four flavivirus infections using Western blot analysis. Based on anti-WNV premembrane antibodies and confirmation by neutralization test, we report three Nicaraguan children with WNV infection, corresponding to a seropositive rate of 7.5%. Our findings underscore the transmission of WNV in humans in Central America and the application of improved seroepidemiological tools to address the knowledge gaps on the prevalence and distribution of WNV in Latin America and the Western Hemisphere.'}]
Zheng Y, Caron DP, Kim JY, Jun SH, Tian Y, Mair F, Stuart KD, Sims PA, Gottardo R
Nature communications
2025-07-01
PMID: 40595741
Antibodies
Columbia University
COVID-19
Epitopes
Gene Expression Profiling
High-Throughput Nucleotide Sequencing
HIPC 2 (2015)
HIPC 3 (2022)
Humans
Membrane Proteins
Seattle Children's Research Institute
Single-Cell Analysis
Transcriptome
Abstract:
Cellular Indexing of Transcriptomes and Epitopes by Sequencing (CITE-seq) enables paired measurement of surface protein and mRNA expression in single cells using antibodies conjugated to oligonucleotide tags. Due to the high copy number of surface protein molecules, sequencing antibody-derived tags (ADTs) allows for robust protein detection, improving cell-type identification. However, variability in antibody staining leads to batch effects in the ADT expression, obscuring biological variation, reducing interpretability, and obstructing cross-study analyses. Here, we present ADTnorm, a normalization and integration method designed explicitly for ADT abundance. Benchmarking against 14 existing scaling and normalization methods, we show that ADTnorm accurately aligns populations with negative- and positive-expression of surface protein markers across 13 public datasets, effectively removing technical variation across batches and improving cell-type separation. ADTnorm enables efficient integration of public CITE-seq datasets, each with unique experimental designs, paving the way for atlas-level analyses. Beyond normalization, ADTnorm includes built-in utilities to aid in automated threshold-gating as well as assessment of antibody staining quality for titration optimization and antibody panel selection. Applying ADTnorm to an antibody titration study, a published COVID-19 CITE-seq dataset, and a human hematopoietic progenitors study allowed for identifying previously undetected phenotype-associated markers, illustrating a broad utility in biological applications.
Johnson MM, Kaushik A, Kline OA, Smith EM, Zhou X, Pat Y, Buergi L, Aguilera J, Alkotob S, Simonin EM, Favaro A, Couto M, Bennett O, Chinthrajah RS, Parsons E, Shamji M, Burke M, Bondy M, Akdis M, Akdis CA, Nadeau KC
Nature medicine
2025-06-26
PMID: 40571754
HIPC 3 (2022)
Stanford
Abstract:
Exposure to fire smoke has become a global health concern and is associated with increased morbidity and mortality. There is a lack of understanding of the specific immune mechanisms involved in smoke exposure, with preventive and targeted interventions needed. After exposure to fire smoke, which includes PM2.5, toxic metals and perfluoroalkyl and polyfluoroalkyl substances, epidemiology-based studies have demonstrated increases in respiratory (for example, asthma exacerbation), cardiac (for example, myocardial infarction, arrhythmias), neurological (for example, stroke) and pregnancy-related (for example, low birthweight, premature birth) outcomes. However, mechanistic studies exploring how smoke exposure disrupts cellular homeostasis are lacking. Therefore, we collected blood from smoke-exposed individuals (n = 31) and age-matched and sex-matched non-smoke-exposed controls (n = 29), and investigated these complex interactions using a single-cell exposomic approach based on both methylation and mass cytometry. Overall, our data demonstrated a strong association between smoke exposure and methylation at 133 disease-relevant gene loci, while immunophenotyping showed increased homing and activation biomarkers. We developed an application of mass cytometry to analyze single-cell/metal binding and found, for example, increased levels of mercury in dead cells and cadmium in the live and dead cell populations. Moreover, mercury levels were associated with years of smoke exposure. Several epigenetic sites across multiple chromosomes were associated with individual toxic metal isotopes in single immune cells. Our methods for detecting the effect of smoke exposure at the single-cell level and the study results may help to determine the timing of exposure and identify specific molecular targets that could be modified to prevent and manage exposure to smoke.
Langelier C, Glascock A, Maguire C, Van Phan H, Lydon E, Calfee C, Corry D, Kheradmand F, Baden L, Sekaly RP, McComsey G, Haddad E, Cairns C, Pulendran B, Fernandez-Sesma A, Simon V, Metcalf J, Higuita N, Messer W, Davis M, Nadeau KC, Kraft M, Bime C, Schaenman J, Erle D, ...
Research square
2025-06-20
PMID: 40585204
HIPC 1 (2010)
HIPC 2 (2015)
HIPC 3 (2022)
Yale University
Abstract:
Azithromycin is often prescribed unnecessarily for respiratory infections, many of which are viral. During the COVID-19 pandemic, its use was widespread, in part due to alleged therapeutic benefits, which have since been disproven. Here, we sought to understand the impact of azithromycin exposure on the respiratory microbiome, antimicrobial resistome, and host immune response in a prospective multicenter cohort of 1164 patients hospitalized for SARS-CoV-2 infection. Using longitudinal nasal metatranscriptomics, we compared patients treated with azithromycin (n=366, 31.4%) to those who received no antibiotics (n=474, 40.7%) or antibiotics other than azithromycin (n=324, 27.8%). We found that azithromycin treatment altered the community composition of the nasal microbiome, reducing bacterial relative abundance, increasing fungal relative abundance, and increasing potentially pathogenic taxa such as Klebsiellaand Staphylococcus. Azithromycin treatment was most notably associated with increases in the number of detectably expressed macrolide/lincosamide/streptogramin (MLS) antimicrobial resistance genes, as well as their relative proportion in the resistome, with changes observable after one day of exposure. Of the MLS resistance genes, the expression of ermC, msrA and ermX increased the most in patients receiving azithromycin. Correlation analyses demonstrated that MLS resistance gene expression was significantly associated with the abundance of several taxa, including both commensal (e.g., Dolosigranulum, Corynebacterium) and potentially pathogenic genera (e.g., Streptococcus, Staphylococcus). Assessment of the peripheral blood and upper airway host transcriptome demonstrated no differences in the expression of inflammatory genes. Taken together, our findings demonstrate that azithromycin treatment in COVID-19 leads to dysbiosis of the upper respiratory microbiome and changes in the expression of MLS resistance genes, without apparent anti-inflammatory benefit.
Kearns K, Lewis SA, Yu ED, Abawi A, Wang E, Maiche S, Mondal M, Vijayanand P, Seumois G, Peters B, Sette A, Da Silva Antunes R
JCI insight
2025-06-09
PMID: 40244697
Adult
Allergens
Animals
Cockroaches
Female
Gene Expression Profiling
HIPC 2 (2015)
HIPC 3 (2022)
Humans
Hypersensitivity
Interferon-gamma
La Jolla Institute for Immunology
Lymphocyte Activation
Male
Mice
Receptors, Antigen, T-Cell, gamma-delta
Single-Cell Analysis
Transcriptome
Abstract:
The role of gamma-delta T (γδ T) cells in immune responses to common allergens is poorly understood. Here, we utilized single-cell (sc) transcriptomic analysis of allergen-reactive γδ T cells in humans to characterize the transcriptional landscapes and TCR repertoires in response to cockroach (CR) and mouse (MO) allergens. Using a potentially novel activation-induced marker (AIM) assay that allows detection of γδ T cells combined with scRNA sequencing and TCR repertoire analysis, we identified both shared and allergen-specific γδ T cell activation patterns and gene expression profiles. While CR extract activated both Vδ1 and Vδ2 subsets, MO extract primarily stimulated Vδ2 cells. Our analysis revealed allergen-specific clusters with distinct functional signatures, including enhanced inflammatory responses and cytotoxic effector functions in MO-specific γδ T cells and natural killer cell-mediated immunity and IFN-γ signaling in CR-specific populations. Comparison of allergic and nonallergic individuals highlighted differences in gene expression and TCR repertoires, including a higher IFNG expression in the CR-allergic compared with nonallergic cohorts, suggesting that phenotypic and functional differences are associated with γδ T allergen responses. This study provides insights into the cellular and molecular heterogeneity and functionality of allergen-reactive γδ T cells, offering a foundation for understanding their role in allergic diseases and potential therapeutic interventions.
Ratnasiri K, Mach SN, Blish CA, Khatri P
bioRxiv : the preprint server for biology
2025-06-08
PMID: 40501846
HIPC 3 (2022)
Stanford
Abstract:
Traditional differential gene expression methods are limited for analysis of single cell RNA-sequencing (scRNA-seq) studies that use paired repeated measures and matched cohort designs. Many existing approaches consider cells as independent samples, leading to high false positive rates while ignoring inherent sampling structures. Although pseudobulk methods address this, they ignore intra-sample expression variability and have higher false negatives rates. We propose a novel meta-analysis approach that accounts for biological replicates and cell variability in paired scRNA-seq data. Using both real and synthetic datasets, we show that our method, single-cell MetaIntegrator (https://github.com/Khatri-Lab/scMetaIntegrator), provides robust effect size estimates and reproducible p-values.
Doni Jayavelu N, Qi JJ, Fourati S, Kheradmand F, Langelier CR, Ehrlich LIR, Diray-Arce J, Hoch A, Kraft M, Becker PM, Altman MC, Montgomery RR
American journal of respiratory cell and molecular biology
2025-06-01
PMID: 40444914
HIPC 1 (2010)
HIPC 2 (2015)
HIPC 3 (2022)
Yale University
Abstract:
None
Yin X, Pu Y, Yuan S, Pache L, Churas C, Weston S, Riva L, Simons LM, Cisneros WJ, Clausen T, Biddle G, Doss-Gollin S, Deming M, De Jesus PD, Kim HN, Fuentes D, Whitelock JM, Esko JD, Lord MS, Mena I, García-Sastre A, Hultquist JF, Frieman MB, Ideker T, Pratt D, ...
PLoS biology
2025-06-01
PMID: 40504864
Animals
COVID-19
HIPC 2 (2015)
Host-Pathogen Interactions
Humans
Proteomics
RNA, Small Interfering
SARS-CoV-2
Virus Replication
Abstract:
Defining the subset of cellular factors governing SARS-CoV-2 replication can provide critical insights into viral pathogenesis and identify targets for host-directed antiviral therapies. While a number of genetic screens have previously reported SARS-CoV-2 host dependency factors, most of these approaches relied on utilizing pooled genome-scale CRISPR libraries, which are biased toward the discovery of host proteins impacting early stages of viral replication. To identify host factors involved throughout the SARS-CoV-2 infectious cycle, we conducted an arrayed genome-scale siRNA screen. Resulting data were integrated with published functional screens and proteomics data to reveal (i) common pathways that were identified in all OMICs datasets-including regulation of Wnt signaling and gap junctions, (ii) pathways uniquely identified in this screen-including NADH oxidation, or (iii) pathways supported by this screen and proteomics data but not published functional screens-including arachionate production and MAPK signaling. The identified proviral host factors were mapped into the SARS-CoV-2 infectious cycle, including 32 proteins that were determined to impact viral replication and 27 impacting late stages of infection, respectively. Additionally, a subset of proteins was tested across other coronaviruses revealing a subset of proviral factors that were conserved across pandemic SARS-CoV-2, epidemic SARS-CoV-1 and MERS-CoV, and the seasonal coronavirus OC43-CoV. Further studies illuminated a role for the heparan sulfate proteoglycan perlecan in SARS-CoV-2 viral entry and found that inhibition of the non-canonical NF-kB pathway through targeting of BIRC2 restricts SARS-CoV-2 replication both in vitro and in vivo. These studies provide critical insight into the landscape of virus-host interactions driving SARS-CoV-2 replication as well as valuable targets for host-directed antivirals.
Load more...