Biology subjects

Wang, J.

Publications and source records attributed to Wang, J..

At least 1,135 records · Page 63Linked to original sources

bioRxiv2024

Versican controlled by Lmx1b regulates hyaluronate density and hydration for semicircular canal morphogenesis

During inner ear semicircular canal morphogenesis in zebrafish, patterned canal-genesis zones express genes for extracellular matrix component synthesis. These include hyaluronan and the hyaluronan-binding chondroitin sulfate proteoglycan Versican, which are abundant in the matrices of many developing organs. Charged hyaluronate polymers play a key role in canal morphogenesis through osmotic swelling. However, the developmental factor(s) that control the synthesis of the matrix components and regulation of hyaluronate density and swelling are unknown. Here, we identify the transcription factor, Lmx1b, as a positive transcriptional regulator of hyaluronan, Versican, and chondroitin synthesis genes crucial for canal morphogenesis. We show that Versican regulates hyaluronan density through its protein core, whereas the charged chondroitin side chains contribute to the osmotic swelling of hyaluronate. Versican-tuned properties of hyaluronate matrices may be a broadly used mechanism in morphogenesis with important implications for understanding diseases where these matrices are impaired, and for hydrogel engineering for tissue regeneration. Summary StatementHere, we reveal the function of the hyaluronan-binding proteoglycan, Versican, and its chondroitin sulfate side chains in tuning the density and hydration of the hyaluronate-rich ECM to generate force, under the control of the transcription factor Lmx1b for successful inner ear semicircular canal morphogenesis in zebrafish.

developmental biology↗

bioRxiv2024

Multi-omics Reveals Immune Response and Metabolic Profiles during High-Altitude Mountaineering

The physiological perturbations induced by high-altitude exposure in mountain climbers, manifesting as metabolic and immunologic deviations, have been previously reported but are not fully understood. In this study, we obtained longitudinal multi-omic profiles of blood samples for healthy mountain climbers during two mountaineering stages (acclimatization and extreme altitude mountaineering). Our integrative assay included metabolomics and lipidomics profiling of plasma coupled with single-cell transcriptomic analysis of 375,722 immune cells. Longitudinal analysis revealed dynamic immune response profiles, during the acclimatization period, characterized by the downregulation of inflammatory responses in monocytes and classical dendritic cells (cDCs) and an increase in the proportion of cytotoxic CD8+ T cells with enhanced immune effector processes. In contrast, during extreme altitude mountaineering, the activation of inflammatory responses and impairment of T cell effector function were observed, concomitant with an increased cellular response to hypoxia and oxidative stress pathways. Furthermore, we found upregulated glycolysis and antioxidant gene expression during extreme altitude mountaineering, which was primarily orchestrated by HIF1A and NFE2L2, while decreased expression of these genes was observed in dysregulated plasmacytoid dendritic cells (pDCs). Finally, high-resolution plasma metabolic analysis revealed significant alterations in the metabolism of climbers, involving enhanced glutamine and fatty acid metabolism.

bioinformatics↗

bioRxiv2024

MoLst8 regulates autophagy and lipid homeostasis in Magnaporthe oryzae

TOR, a widely conserved eukaryotic protein kinase, forms TORC1 and TORC2 to regulate diverse cell signaling. TORC1 controls protein synthesis, cell cycle, and autophagy, whereas TORC2 manages cell polarity, cytoskeleton, and membrane structure. Our previous research found that MoVast2, along with MoVast1, regulates TOR in rice blast fungus Magnaporthe oryzae, maintaining lipid and autophagy balance. Lst8, a key TOR complex component in yeast and mammalian cells. However, the precise role of MoLst8 in M. oryzae is still unclear. In this study, we obtained the {Delta}Molst8 mutant through high-through gene knockout strategies. The results showed that loss of MoLST8 leading to a series of defects, such as growth and sporulation reduction, abnormal conidia, and loss of virulence. In addition, this mutant is highly sensitive to rapamycin, leading to growth arrest and autophagy impairment, indicated that MoLst8 positively regulates TORC1 for cellular growth, metabolism, and autophagy. Lipidomics analysis in the mutant revealed lipid metabolism dysregulation, sphingolipid reduction, disrupting membrane tension and homeostasis, suggested that TORC2 mediated lipid regulation is disordered in {Delta}Molst8 mutant. Additionally, the study explored TOR-MAPK crosstalk, finding that the mutant shows heightened cell wall stress sensitivity but fails to restore integrity despite MAPK activation. These findings offer insights into MoLst8s role in fungal pathogenesis, contributing to an understanding of fungal biology and disease control strategies.

microbiology↗

bioRxiv2024

Estropausal gut microbiota transplant improves ovarian function in adult mice

Decline in ovarian function with age not only affects fertility but is also linked to a higher risk of age-related diseases in women (e.g. osteoporosis, dementia). Intriguingly, earlier menopause is linked to shorter lifespan; however, the underlying molecular mechanisms of ovarian aging are not well understood. Recent evidence suggests the gut microbiota may influence ovarian health. In this study, we characterized ovarian aging associated microbial profiles in mice and investigated the effect of the gut microbiome from young and estropausal female mice on ovarian health through fecal microbiota transplantation. We demonstrate that the ovarian transcriptome can be broadly remodeled after heterochronic microbiota transplantation, with a reduction in inflammation-related gene expression and trends consistent with transcriptional rejuvenation. Consistently, these mice exhibited enhanced ovarian health and increased fertility. Using metagenomics-based causal mediation analyses and serum untargeted metabolomics, we identified candidate microbial species and metabolites that may contribute to the observed effects of fecal microbiota transplantation. Our findings reveal a direct link between the gut microbiota and ovarian health.

physiology↗

bioRxiv2024

Development of the overlapping network modules in the human brain

Developmental connectomic studies have shown that the modular organization of functional networks in the human brain undergoes substantial reorganization with age to support cognitive growth. However, these studies implicitly assume that each brain region belongs to one and only one specific network module, ignoring the potential spatial overlap between functional modules. How the overlapping functional modular architecture develops and whether this development is related to structural signatures remain unknown. Using longitudinal multimodal structural, functional, and diffusion MRI data from 305 children (aged 6-14 years), we investigated the development of the overlapping modular architecture of functional networks, and further explored their structural associations. Specifically, an edge-centric network model was used to identify the overlapping functional modules, and the nodal overlap in module affiliations was quantified using the entropy measure. We showed a remarkable regional inhomogeneity in module overlap in children, with higher entropy in the ventral attention, somatomotor, and subcortical networks and lower entropy in the visual and default-mode networks. Furthermore, the overlapping modules developed in a linear, spatially dissociable manner from childhood to adolescence, with significantly reduced entropy in the prefrontal cortex and putamen and increased entropy in the parietal lobules. Personalized overlapping modular patterns capture individual brain maturity as characterized by brain age. Finally, the overlapping functional modules can be significantly predicted by integrating gray matter morphology and white matter network properties. Our findings highlight the maturation of overlapping network modules and their structural substrates, thereby advancing our understanding of the principles of connectome development.

neuroscience↗

bioRxiv2024

Protection of savings by reducing the salience of opposing errors

When humans encounter the same perturbation twice, they typically adapt faster the second time, a phenomenon called savings. Studies have examined savings following adaptation to a gradually introduced perturbation, with mixed results. These inconsistencies might be caused by differences in how behavior returns to its baseline state during the washout phase in between learning periods. To test this, participants controlled a cursor that was subject to a visual rotation in its motion direction. The rotation was applied during two learning periods, separated by a washout period where the rotation was removed abruptly, gradually, or without error feedback. We found that the type of error experienced during washout affected savings: abrupt washout with large errors eliminated savings, whereas gradual or no-feedback washout preserved it. Model-based analyses indicated these effects were driven by changes in error sensitivity suggesting that salient, opposing errors experienced during washout downregulate the response to error, nullifying savings.

neuroscience↗

bioRxiv2024

VGLL2 and TEAD1 fusion proteins drive YAP/TAZ-independent transcription and tumorigenesis by engaging p300

Studies on Hippo pathway regulation of tumorigenesis largely center on YAP and TAZ, the transcriptional co-regulators of TEAD. Here, we present an oncogenic mechanism involving VGLL and TEAD fusions that is Hippo pathway-related but YAP/TAZ-independent. We characterize two recurrent fusions, VGLL2-NCOA2 and TEAD1-NCOA2, recently identified in spindle cell rhabdomyosarcoma. We demonstrate that in contrast to VGLL2 and TEAD1, the fusion proteins are strong activators of TEAD-dependent transcription, and their function does not require YAP/TAZ. Furthermore, we identify that VGLL2 and TEAD1 fusions engage specific epigenetic regulation by recruiting histone acetyltransferase p300 to control TEAD-mediated transcriptional and epigenetic landscapes. We showed that small molecule p300 inhibition can suppress fusion proteins-induced oncogenic transformation both in vitro and in vivo. Overall, our study reveals a molecular basis for VGLL involvement in cancer and provides a framework for targeting tumors carrying VGLL, TEAD, or NCOA translocations.

cancer biology↗

bioRxiv2024

The genetic architecture and evolutionary consequences of the human pelvic form

Human pelvic shape has undergone significant evolutionary change since the divergence from the chimpanzee lineage. This transformation, involving the reduction of the pelvic canal size to support bipedal locomotion, is thought to give rise to the obstetrical dilemma, a hypothesis highlighting the mismatch between the large brain size of infants and the narrowed birth canal in females. Empirical evidence for this classic hypothesis has been equivocal, largely due to a lack of sample size and appropriate types of data. To elucidate the genetic underpinnings of pelvic morphology, we applied a deep learning model to 31,115 dual-energy X-ray absorptiometry (DXA) from the UK Biobank, extracting a set of seven pelvic proportion (PP) phenotypes, including measures of the birth canal. All PPs were found to be highly heritable ([~]25-40%) and a genome-wide association study of these traits identified 179 independent loci. Unlike other skeletal proportions including long bone lengths, the subpubic angle associated with the birth canal exhibits a genetic correlation between sexes significantly less than 1, in line with sex-specific reproductive function. PPs were also left-right asymmetric but not heritable and instead associated with handedness. We conducted phenotypic and genetic association analyses to link PPs to 3 facets of the dilemma: locomotion, pelvic floor function and childbirth. Larger birth canal phenotypes were associated with reduced walking pace, decreased risk of back pain, and increased risk of hip osteoarthritis - phenotypes linked to locomotor efficiency. We also observed that a narrower birth canal width was associated with a reduced risk of pelvic floor disorders. When examining childbirth-related outcomes, narrower birth canal phenotypes were associated with increased risk of emergency cesarean sections and obstructed labor due to insufficient dilation, but not obstructed labor due to positioning of the fetus. Finally, we examined whether the dilemma might have been alleviated through evolution. We found no association between any PPs and gestational duration, contrary to the initial prediction by Washburn in 1960. However, we found that the birth weight of the child, a proxy for skull and brain size, was genetically correlated with birth canal width but not with other PPs. Collectively, our study offers fresh insight on a 60-year-old debate in human evolutionary studies. Our results support the idea that the obstetrical dilemma has played a central role in the co-evolution of the human brain and pelvis, while also highlighting the potential role of associated factors such as pelvic floor health.

genetics↗

bioRxiv2024

Human myogenic progenitor cells display tenogenic differentiation potential and facilitate tendon regeneration

Tendon injury occurs at high frequency and is difficult to repair. Identification of human stem cells being able to regenerate tendon will greatly facilitate the development of regenerative medicine for tendon injury. We identified human CD29+/CD56+ myogenic progenitors having tendon differentiation potential both in vitro and in vivo. Transplantation of human CD29+/CD56+ myogenic progenitors contributes to injured tendon repair and thus improves locomotor function. Interestingly, the tendon differentiation potential in mouse muscle stem cells is minimal and the higher TGF{beta} signaling level may be the key for the distinct feature of human CD29+/CD56+ myogenic progenitors. These findings reveal that human CD29+/CD56+ myogenic progenitors are bi-potential adult stem cells and can serve as a new source for tendon regeneration.

cell biology↗

bioRxiv2024

The alternative splicing of ZmHsf23 regulates heat stress tolerance in maize

O_LIHeat stress is one of the major threats to maize (Zea mays) production globally. Heat shock transcription factors (HSFs) play vital roles in plant heat stress responses. However, the molecular and genetic basis of HSFs in maize thermotolerance remain largely unknown. C_LIO_LIIn this study, we reveal that the alternative splicing of Hsf23 in maize modulates heat stress tolerance. Hsf23 produces two functional transcripts, the full-length transcript Hsf23b and the heat-inducible transcript Hsf23a. The two Hsf23 transcripts differ by the presence of a cryptic mini exon in Hsf23a, which is spliced out in Hsf23b. Both Hsf23a and Hsf23b were intensely expressed in response to heat stress. C_LIO_LIThe overexpression of Hsf23b, not Hsf23a, enhanced heat stress tolerance, while loss-of-function mutations of Hsf23a and Hsf23b exhibited remarkably increased sensitivity to heat stress. Transcriptome analysis revealed that Hsf23b activates broader heat-responsive genes than Hsf23a, and Hsf23a and Hsf23b modulate heat stress response through different downstream targets. Furthermore, Hsf23a physically interacted with Hsf23b and promotes Hsf23b-regulated expression of sHSP genes. C_LIO_LITogether, our finding provides new insights into the roles of ZmHsf23 in the heat tolerance in maize, and presents an important candidate for the genetic improvement of heat-tolerant maize varieties. C_LI

plant biology↗

bioRxiv2024

Curved light sheet microscopy for centimeter-scale cleared tissues imaging

Imaging large cleared tissues requires scaling the throughput of imaging techniques. Here we introduce curved light sheet microscope to perform optical sectioning with curved light sheets. This concept addresses the long-standing field curvature problem and lowers the barriers in designing high-throughput objectives. Leveraging a customized objective, the curved light sheet microscope achieves diffraction-limited resolution (1.0 m laterally and 2.5 m axially) and uniform contrast over a field of view of more than 1 x 1 cm2 and is compatible with various tissue clearing techniques. Imaging an entire intact cleared mouse brain at 0.625 x 0.625 x 1.25 m3 voxel size takes less than 3 hours and image tiling is not required. We share full optics description of the objective and report imaging neuronal and vascular networks and tracing brain-wide long-distance axonal projections in intact mouse brains.

bioengineering↗

bioRxiv2024

Impacts of global warming on fertility of male fishes: evidence from meta-analysis of temperature effects on spermatozoa motility

Studies have demonstrated adverse effects of global warming on aquatic ecosystems from the abiotic to the biotic level. In the present work, a meta-analysis study was conducted to elucidate the effects of global warming on spermatozoa functions, which are key determinants of male fertility. We recruited 245 data records from a pool of empirical studies, which includes 20 studies spanning 20 cold- and warm-water fish species, to identify the effects of increased water temperature (IWT) on determinants of sperm fertility in fishes. Data were systematically re-processed and re-analyzed to determine the overall effects of IWT on sperm kinetics such as motility (MOT), duration of motility (DSM), curvilinear velocity (VCL), rectilinear velocity (VSL) and average path velocity (VAP), as well as on enzymatic activities for energy supply (EAES) and antioxidant enzyme activity (ANEA). The standardized mean difference was calculated for each study, with positive values indicating higher performance under IWT. Results showed that (a) the overall effect size for MOT was more negative in cold-water fishes (-1.22) than in warm-water fishes (-0.98). (b) Each 1 {degrees}C increase in the activation medium reduced MOT by 1.30% (cold-water fishes) and 3.47% (warm-water fishes). (c) The IWT negatively affected DSM, decreasing it by 10 s (cold-water species) and 5.64 s (warm-water species) per degree of IWT. (d) Spermatozoa velocity (VCL and VSL) was increased by IWT in warm-water species. In conclusion, this study shows that IWT negatively affects sperm motility kinetics, suggesting an impact of global warming on fish reproduction.

cell biology↗

bioRxiv2024

CA1i pyramidal neurons mediate the role of NMDA receptor subunit GluN3A in depressive behavior and D-serine anti-depression

The hippocampus is a highly complex structure, defined by profound structural, functional, and molecular heterogeneity. The GluN3A subunit, which forms non-classic N-methyl-D-aspartate receptors (NMDARs), is enriched in the hippocampal CA1 subregion and has a poorly understood functional role, especially in stress-related behavioral regulation. Here, we employed chronic social defeat stress (CSDS) and GluN3A knockout (KO) mouse models combined with behavioral, molecular, genetic, pharmacological, and circuit-level analyses to investigate the role of hippocampal GluN3A in stress coping. We found that CSDS selectively reduced GluN3A expression in the intermediate CA1 (CA1i) region. Decreased GluN3A expression in CA1i, from either stress or genetic deletion, promoted passive coping behaviors, whereas overexpression of GluN3A in CA1i reversed the phenotype under both conditions. Mechanistically, consistent with GluN3A enrichment in pyramidal neurons, c-fos staining and fiber photometry revealed that GluN3A was essential for CA1i pyramidal neuronal activation during coping behaviors. Further chemogenetic manipulations demonstrated that activating CA1i neurons facilitated active coping, while inhibition induced passivity. Moreover, local administration of D-serine, an agonist of GluN3A-containing NMDARs, rapidly shifted coping behavior from passive to active by activating CA1i neurons via GluN3A-dependent mechanisms. Circuit tracing revealed that CA1i neurons project to multiple sub-hippocampal and cortico-limbic regions, and GluN3A overexpression selectively enhanced downstream neuronal activity in CA3 and infralimbic cortex, but not in the nucleus accumbens. Together, these findings identify GluN3A as a key molecule linking hippocampal subregional specialization with adaptive stress coping, and suggest that the rapid, resilience-promoting effects of D-serine are also GluN3A-dependent.

neuroscience↗

bioRxiv2024

CRISPR screens reveal convergent targeting strategies against evolutionarily distinct chemoresistance in cancer

Resistance to chemotherapy has been a major hurdle that limits therapeutic benefits for many types of cancer. Here we systematically identify genetic drivers underlying chemoresistance by performing 30 genome-scale CRISPR knockout screens for seven chemotherapeutic agents in multiple cancer cells. Chemoresistance genes vary between conditions primarily due to distinct genetic background and mechanism of action of drugs, manifesting heterogeneous and multiplexed routes towards chemoresistance. By focusing on oxaliplatin and irinotecan resistance in colorectal cancer, we unravel that evolutionarily distinct chemoresistance can share consensus vulnerabilities identified by 26 second-round CRISPR screens with druggable gene library. We further pinpoint PLK4 as a therapeutic target to overcome oxaliplatin resistance in various models via genetic ablation or pharmacological inhibition, highlighting a single-agent strategy to antagonize evolutionarily distinct chemoresistance. Our study not only provides resources and insights into the molecular basis of chemoresistance, but also proposes potential biomarkers and therapeutic strategies against such resistance.

cancer biology↗

bioRxiv2024

SAMP: Identifying Antimicrobial Peptides by an Ensemble Learning Model Based on Proportionalized Split Amino Acid Composition

AbstractIt is projected that 10 million deaths could be attributed to drug-resistant bacteria infections in 2050. To address this concern, identifying new-generation antibiotics is an effective way. Antimicrobial peptides (AMPs), a class of innate immune effectors, have received significant attention for their capacity to eliminate drug-resistant pathogens, including viruses, bacteria, and fungi. Recent years have witnessed widespread applications of computational methods especially machine learning (ML) and deep learning (DL) for discovering AMPs. However, existing methods only use features including compositional, physiochemical, and structural properties of peptides, which cannot fully capture sequence information from AMPs. Here, we present SAMP, an ensemble random projection (RP) based computational model that leverages a new type of features called Proportionalized Split Amino Acid Composition (PSAAC) in addition to conventional sequence-based features for AMP prediction. With this new feature set, SAMP captures the residue patterns like sorting signals at around both the N-terminus and the C-terminus, while also retaining the sequence order information from the middle peptide fragments. Benchmarking tests on different balanced and imbalanced datasets demonstrate that SAMP consistently outperforms existing state-of-the-art methods, such as iAMPpred and AMPScanner V2, in terms of accuracy, MCC, G-measure and F1-score. In addition, by leveraging an ensemble RP architecture, SAMP is scalable to processing large-scale AMP identification with further performance improvement, compared to those models without RP. To facilitate the use of SAMP, we have developed a Python package freely available at https://github.com/wan-mlab/SAMP.

bioinformatics↗

bioRxiv2024

ATM and 53BP1 regulate alternative end joining-mediated V(D)J recombination

G0/G1-phase alternative end joining (A-EJ) is a recently defined mutagenic pathway characterized by resected deletion and translocation joints that are predominantly direct and are distinguished from A-EJ in cycling cells which rely much more on microhomology-mediated end joining (MMEJ). Using chemical and genetic approaches, we systematically evaluate potential A-EJ factors and DNA damage response (DDR) genes to support this mechanism by mapping the repair fates of RAG1/2-initiated DSBs in the context of Ig{kappa} locus V-J recombination and chromosome translocation. Our findings highlight a polymerase theta-independent Parp1-XRCC1/Lig3 axis as central A-EJ components, supported by 53BP1 in the context of an ATM-activated DDR. Mechanistically, we demonstrate varied changes in short-range resection, MMEJ, and translocation, imposed by compromising specific DDR activities, which include polymerase alpha, ATR, DNA2, and Mre11. This study advances our understanding of DNA damage repair within the 53BP1 regulatory domain and the RAG1/2 post-cleavage complex.

molecular biology↗

bioRxiv2024

Deep, unbiased and quantitative mass spectrometry-based plasma proteome analysis of individual responses to mRNA COVID-19 vaccine

Global campaign against COVID-19 have vaccinated a significant portion of the world population in recent years. Combating the COVID-19 pandemic with mRNA vaccines played a pivotal role in the global immunization effort. However, individual responses to a vaccine are diverse and lead to varying vaccination efficacy. Despite significant progress, a complete understanding of the molecular mechanisms driving the individual immune response to the COVID-19 vaccine remains elusive. To address this gap, we combined a novel nanoparticle-based proteomic workflow with tandem mass tag (TMT) labeling, to quantitatively assess the proteomic changes in a cohort of 12 volunteers following two doses of the Pfizer-BioNTech mRNA COVID-19 vaccine. This optimized protocol seamlessly integrates comprehensive proteome analysis with enhanced throughput by leveraging the enrichment of low-abundant plasma proteins by engineered nanoparticles. Our data demonstrate the ability of this nanoparticle-based workflow to quantify over 3,000 proteins from 48 human plasma samples, providing the deepest view into COVID-19 vaccine-related plasma proteome study. We identified 69 proteins exhibiting a boosted response to the vaccine after the second dose. Additionally, 74 proteins were differentially regulated between seven volunteers, who contracted COVID-19 despite receiving two doses of the vaccine, and the ones who did not contract COVID-19. These findings offer valuable insights into individual variability in response to vaccination, demonstrating the potential of personalized medicine approaches in vaccine development.

immunology↗

bioRxiv2024

Humoral immunogenicity comparison of XBB and JN.1 in human infections

The continuous evolution of SARS-CoV-2, particularly the emergence of the BA.2.86/JN.1 lineage replacing XBB lineages, necessitates re-evaluation of current vaccine compositions. Here, we provide a comprehensive analysis of the humoral immune response to XBB and JN.1 human exposures, emphasizing the need for JN.1-lineage-based boosters. We demonstrate the antigenic distinctiveness of XBB and JN.1 lineages in SARS-CoV-2-naive individuals but not in those with prior vaccinations or infections, and JN.1 infection elicits superior plasma neutralization titers against its subvariants. We highlight the strong immune evasion and receptor binding capability of KP.3, supporting its foreseeable prevalence. Extensive analysis of the BCR repertoire, isolating [~]2000 RBD-specific monoclonal antibodies (mAbs) with their targeting epitopes characterized by deep mutational scanning (DMS), underscores the systematic superiority of JN.1-elicited memory B cells (MBCs). Notably, Class 1 IGHV3-53/3-66-derived neutralizing antibodies (NAbs) contribute majorly within wildtype (WT)-reactive NAbs against JN.1. However, KP.2 and KP.3 evade a substantial subset of them, even those induced by JN.1, advocating for booster updates to KP.3 for optimized enrichment. JN.1-induced Omicron-specific antibodies also demonstrate high potency across all Omicron lineages. Escape hotspots of these NAbs have mainly been mutated in Omicron RBD, resulting in higher immune barrier to escape, considering the probable recovery of previously escaped NAbs. Additionally, the prevalence of broadly reactive IGHV3-53/3-66- encoding antibodies and MBCs, and their capability of competing with all Omicron-specific NAbs suggests their inhibitory role on the de novo activation of Omicron-specific naive B cells, potentially explaining the heavy immune imprinting in mRNA-vaccinated individuals. These findings delineate the evolving antibody response to Omicron antigenic shift from XBB to JN.1, and highlight the importance of developing JN.1 lineage, especially KP.3-based vaccine boosters, to enhance humoral immunity against current and future SARS-CoV-2 variants.

immunology↗