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12,799 results for “Immunization”
Data from: A nanovaccine for immune activation and prophylactic protection of atherosclerosis in mouse models
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Mass spectrometry data from: Deficiency in Galectin-3, -8, and -9 impairs immunity to chronic Mycobacterium tuberculosis infection but not acute infection with multiple intracellular pathogens
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Strains and constructs for: A chimeric nuclease substitutes a phage CRISPR-Cas system to provide sequence specific immunity against subviral parasites
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Long COVID manifests with T cell dysregulation, inflammation, and an uncoordinated adaptive immune response to SARS-CoV-2
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Dataset related to article "Single-Cell Sequencing of Mouse Heart Immune Infiltrate in Pressure Overload-Driven Heart Failure Reveals Extent of Immune Activation."
<p>BACKGROUND:</p> <p>Inflammation is a key component of cardiac disease, with macrophages and T lymphocytes mediating essential roles in the progression to heart failure. Nonetheless, little insight exists on other immune subsets involved in the cardiotoxic response.</p> <p>METHODS:</p> <p>Here, we used single-cell RNA sequencing to map the cardiac immune composition in the standard murine nonischemic, pressure-overload heart failure model. By focusing our analysis on CD45<sup>+</sup> cells, we obtained a higher resolution identification of the immune cell subsets in the heart, at early and late stages of disease and in controls. We then integrated our findings using multiparameter flow cytometry, immunohistochemistry, and tissue clarification immunofluorescence in mouse and human.</p> <p>RESULTS:</p> <p>We found that most major immune cell subpopulations, including macrophages, B cells, T cells and regulatory T cells, dendritic cells, Natural Killer cells, neutrophils, and mast cells are present in both healthy and diseased hearts. Most cell subsets are found within the myocardium, whereas mast cells are found also in the epicardium. Upon induction of pressure overload, immune activation occurs across the entire range of immune cell types. Activation led to upregulation of key subset-specific molecules, such as oncostatin M in proinflammatory macrophages and PD-1 in regulatory T cells, that may help explain clinical findings such as the refractivity of patients with heart failure to anti-tumor necrosis factor therapy and cardiac toxicity during anti-PD-1 cancer immunotherapy, respectively.</p> <p>CONCLUSIONS:</p> <p>Despite the absence of infectious agents or an autoimmune trigger, induction of disease leads to immune activation that involves far more cell types than previously thought, including neutrophils, B cells, Natural Killer cells, and mast cells. This opens up the field of cardioimmunology to further investigation by using toolkits that have already been developed to study the aforementioned immune subsets. The subset-specific molecules that mediate their activation may thus become useful targets for the diagnostics or therapy of heart failure.</p> <p> </p> <p>This dataset is created in .ets form, we attach a pdf with the information about.</p>
Dataset related to article "Costimulatory Molecules and Immune Checkpoints Are Differentially Expressed on Different Subsets of Dendritic Cells."
<p>Dendritic cells (DCs) play a crucial role in initiating and shaping immune responses. The effects of DCs on adaptive immune responses depend partly on functional specialization of distinct DC subsets, and partly on the activation state of DCs, which is largely dictated by environmental signals. Fully activated immunostimulatory DCs express high levels of costimulatory molecules, produce pro-inflammatory cytokines, and stimulate T cell proliferation, whereas tolerogenic DCs express low levels of costimulatory molecules, produce immunomodulatory cytokines and impair T cell proliferation. Relevant to the increasing use of immune checkpoint blockade in cancer treatment, signals generated from inhibitory checkpoint molecules on DC surface may also contribute to the inhibitory properties of tolerogenic DCs. Yet, our knowledge on the expression of inhibitory molecules on human DC subsets is fragmentary. Therefore, in this study, we investigated the expression of three immune checkpoints on peripheral blood DC subsets, in basal conditions and upon exposure to pro-inflammatory and anti-inflammatory stimuli, by using a flow cytometric panel that allows a direct comparison of the activatory/inhibitory phenotype of DC-lineage and inflammatory DC subsets. We demonstrated that functionally distinct DC subsets are characterized by differential expression of activatory and inhibitory molecules, and that cDC1s in particular are endowed with a unique immune checkpoint repertoire characterized by high TIM-3 expression, scarce PD-L1 expression and lack of ILT2. Notably, this unique cDC1 repertoire was subverted in a group of patients with myelodysplastic syndromes included in the study. Applied to the characterization of DCs in the tumor microenvironment, this panel has the potential to provide valuable information to be used for investigating the role of DC subsets in cancer, guiding DC-targeting treatments, and possibly identifying predictive biomarkers for clinical response to cancer immunotherapy.</p>
IL4I1 Is a Metabolic Immune Checkpoint that Activates the AHR and Promotes Tumor Progression
<p>These data objects were generated for the manuscript " IL4I1 Is a Metabolic Immune Checkpoint that Activates the AHR and Promotes Tumor Progression".</p>
Data from: Reprograming of epigenetic mechanisms controlling host insect immunity and development in response to egg-laying by a parasitoid wasp
<p>Parasitoids are insects that use other insects as hosts. They sabotage host cellular and humoral defenses to promote the survival of their offspring by injecting viruses and venoms along with their eggs. Many pathogens and parasites disrupt host epigenetic mechanisms to overcome immune system defenses, and we hypothesized that parasitoids may utilize the same strategy. We used the ichneumon wasp Pimpla turionellae as a model idiobiont parasitoid to test this hypothesis, with pupae of the greater wax moth Galleria mellonella as the host. We found that parasitoid infestation involves the suppression of host immunity-related effector genes and the modulation of host genes involved in developmental hormone signaling. The transcriptional reprogramming of host genes following the injection of parasitoid eggs was associated with changes in host epigenetic mechanisms. The introduction of parasitoids resulted in a transient decrease in host global DNA methylation and the modulation of acetylation ratios for specific histones. Genes encoding regulators of histone acetylation and deacetylation were mostly downregulated in the parasitized pupae, suggesting that parasitoids can suppress host transcription. We also detected a strong parasitoid-specific effect on host microRNAs regulating gene expression at the post-transcriptional level. Our data therefore support the hypothesis that parasitoids may favor the survival of their offspring by interfering with host epigenetic mechanisms to suppress the immune system and disrupt development.</p>
Data from: How qualified immunity fails
<p>This Article reports the findings of the largest and most comprehensive study to date of the role qualified immunity plays in constitutional litigation. Qualified immunity shields government officials from constitutional claims for money damages so long as the officials did not violate clearly established law. The Supreme Court has described the doctrine as incredibly strong—protecting "all but the plainly incompetent or those who knowingly violate the law." Legal scholars and commentators describe qualified immunity in equally stark terms, often criticizing the doctrine for closing the courthouse doors to plaintiffs whose rights have been violated. The Court has repeatedly explained that qualified immunity must be as powerful as it is to protect government officials from burdens associated with participating in discovery and trial. Yet the Supreme Court has relied on no empirical evidence to support its assertion that qualified immunity doctrine shields government officials from these assumed burdens.</p> <p>This Article is the first to test this foundational assumption underlying the Supreme Court's qualified immunity decisions. I reviewed the dockets of 1,183 Section 1983 cases filed against state and local law enforcement defendants in five federal court districts over a two-year period and measured the frequency with which qualified immunity motions were brought by defendants, granted by courts, and dispositive before discovery and trial. I found that qualified immunity rarely served its intended role as a shield from discovery and trial in these cases. Across the five districts in my study, just thirty-eight (3.9%) of the 979 cases in which qualified immunity could be raised were dismissed on qualified immunity grounds. And when one considers all the Section 1983 cases brought against law enforcement defendants—each of which could expose law enforcement officials to burdens associated with discovery and trial—just seven (0.6%) were dismissed at the motion to dismiss stage and thirty-one (2.6%) were dismissed at summary judgment on qualified immunity grounds. My findings enrich our understanding of qualified immunity's role in constitutional litigation, belie expectations about the policy interests served by qualified immunity, and show that qualified immunity doctrine should be modified to reflect its actual role in constitutional litigation.</p>
Data from: Sustained immune activation is associated with susceptibility to the amphibian chytrid fungus
The disease chytridiomycosis caused by the fungus Bd has devastated amphibian populations worldwide. Functional genomic contributions to host susceptibility remain enigmatic and vary between species and populations. We conducted experimental Bd infections in Rana yavapaiensis, a species with intraspecific variation in chytridiomycosis susceptibility, to assess the skin and spleen transcriptomic response to infection over time. We predicted that increased immune gene expression would be associated with a positive disease outcome, but we instead found that surviving frogs had significantly reduced immune gene expression compared to susceptible frogs and to uninfected controls. MHC class II gene expression was also significantly higher in susceptible frogs compared to surviving frogs. Furthermore, susceptible frogs expressed a significantly larger number of distinct class II alleles, demonstrating a negative correlation between class II expression, functional diversity, and survival. Expression of the MHC class II locus previously associated with Bd disease outcomes was a significant predictor of Bd infection intensity at early infection stages but not at late infection stages, suggesting initial MHC-linked immune processes are important for ultimate disease outcomes. We infer through disease association and phylogenetic analysis that certain MHC variants are linked to the immune expression that was negatively associated with survival, and we hypothesize that frogs that did not express these alleles could better survive infections. Our study finds that MHC expression at early and late infection stages predicts Bd infection intensity, and suggests that generating a sustained immune response against Bd may be counterproductive for surviving chytridiomycosis in this partially susceptible species.
Data from: Social effects on age-related and sex-specific immune cell profiles in a wild mammal
<p>Evidence for age-related changes in innate and adaptive immune responses is increasing in wild populations. Such changes have been linked to fitness, and knowledge of the factors driving immune response variation is important for understanding the evolution of immunity. Age-related changes in immune profiles may be due to factors such as immune system development, sex-specific behaviour and responses to environmental conditions. Social environments may also contribute to variation in immunological responses, for example, through transmission of pathogens and stress arising from resource and mate competition. Yet, the impact of the social environment on age-related changes in immune cell profiles is currently understudied in the wild. Here, we tested the relationship between leukocyte cell composition (proportion of neutrophils and lymphocytes [innate and adaptive immunity, respectively] that were lymphocytes) and age, sex, and group size in a wild population of European badgers (<i>Meles meles</i>). We found that the proportion of lymphocytes in early-life was greater in males in smaller groups compared to larger groups, but with a faster age-related decline in smaller groups. In contrast, the proportion of lymphocytes in females was not significantly related to age or group size. Our results provide evidence of sex-specific age-related changes in immune cell profiles in a wild mammal, which are influenced by the social environment.</p>
Reproduction affects immune defenses in the guinea pig even under ad libitum food
<p>Reproduction is one of the most costly processes in the life of an animal. Life history theory assumes that when resources are limiting allocation to reproduction will reduce allocation to other essential processes thereby inducing costs of reproduction. The immune system is vital for survival. If reproduction reduces investment in immune function, this could increase the risk of disease, morbidity and mortality. We here test in the guinea pig, if even under <i>ad libitum</i> food conditions, pregnancy and lactation reduce the activity of the adaptive and innate immune system compared to the reaction of non-reproducing animals. In response to a challenge with keyhole limpet haemocyanin the antibody-mediated adaptive immunity during pregnancy and lactation was reduced. Pregnant and lactating females showed higher levels of bacterial killing activity, an integrated measure of innate immunity, than non-reproducing females. However, two major effectors of the innate immunity, the natural antibody and the complement of pregnant and lactating females showed lower levels than in non-reproducing females. Pregnant and lactating females did not differ significantly in the expressed levels of innate immunity. Our results indicate that changes in the immune response during reproduction are physiological adjustments to predictable allocation problems, because they happen even under <i>ad libitum</i> food availability.</p>
Noninvasive measurement of mucosal immunity in a free‐ranging baboon population
<p>Ecoimmunological patterns and processes remain understudied in wild primates, in part because of the lack of noninvasive methods to measure immunity. Secretory immunoglobulin A (sIgA) is the most abundant antibody present at mammalian mucosal surfaces and provides an important first line of defense against pathogens. Recent studies show that sIgA can be measured noninvasively in feces and is a good marker of mucosal immunity. Here we validated a commercial ELISA kit to measure fecal IgA in baboons, tested the robustness of its results to variation in collection and storage conditions, and developed a cost‐effective in‐house ELISA for baboon fecal IgA. Using data from the custom ELISA, we assessed the relationship between fecal IgA concentrations and gastrointestinal parasite burden, and tested how sex, age, and reproductive effort predict fecal IgA in wild baboons. We find that IgA concentrations can be measured in baboon feces using an in‐house ELISA and are highly correlated to the values obtained with a commercial kit. Fecal IgA concentrations are stable when extracts are stored for up to 22 months at −20°C. Fecal IgA concentrations were negatively correlated with parasite egg counts (Trichuris trichiura), but not parasite richness. Fecal IgA did not vary between the sexes, but for males, concentrations were higher in adults versus adolescents. Lactating females had significantly lower fecal IgA than pregnant females, but neither pregnant nor lactating female concentrations differed significantly from cycling females. Males who engaged in more mate‐guarding exhibited similar IgA concentrations to those who engaged in little mate‐guarding. These patterns may reflect the low energetic costs of mucosal immunity, or the complex dependence of IgA excretion on individual condition. Adding a noninvasive measure of mucosal immunity will promote a better understanding of how ecology modulates possible tradeoffs between the immune system and other energetically costly processes in the wild.</p>
Longitudinal Saliva Omics Responses to Immune Perturbation: A Case Study
<p>Online Data Files [ODFs] accompanying manuscript "Longitudinal Saliva Omics Responses to Immune Perturbation: A Case Study"</p>
The impacts of body mass on immune cell concentrations in birds
<p>Body mass affects many biological traits, but its impacts on immune defenses are fairly unknown. Recent research on mammals found that neutrophil concentrations disproportionately increased (scaled hypermetrically) with body mass, a result not predicted by any existing theory. Although the scaling relationship for mammals might predict how leukocyte concentrations scale with body mass in other vertebrates, vertebrate classes are distinct in many ways that might affect their current and historic interactions with parasites and hence the evolution of their immune systems. Subsequently, here, we asked which existing scaling hypothesis best-predicts relationships between body mass and lymphocyte, eosinophil, and heterophil concentrations—the avian functional equivalent of neutrophils—among >100 species of birds. We then examined the predictive power of body mass relative to life-history variation, as an extensive literature indicates that the timing of key life events has influenced immune system variation among species. Finally, we ask whether avian scaling patterns differ from the patterns we observed in mammals. We found that an intercept-only model best-explained lymphocyte and eosinophil concentrations among birds, indicating that the concentrations of these cell types were both independent of body mass. For heterophils, however, body mass explained 31% of the variation in concentrations among species, much more than life-history variation (4%). As with mammalian neutrophils, avian heterophils scaled hypermetrically (<i>b=</i>0.19 +/- 0.05), but more steeply than mammals (~1.5x; 0.11+/- 0.03). As such, we discuss why birds might require more broadly-protective cells compared to mammals of the same body size. Overall, body mass appears to have strong influences on the architecture of immune systems.</p>
Data from: Habitat fragmentation differentially shapes neutral and immune gene variation in a tropical bird species
<p>Habitat fragmentation is a major cause of biodiversity loss, responsible for an alteration of intraspecific patterns of neutral genetic diversity and structure. Although neutral genetic variation can be informative for demographic inferences, it may be a poor predictor of adaptive genetic diversity and thus of the consequences of habitat fragmentation on selective evolutionary processes. In this context, we contrasted patterns of genetic diversity and structure of neutral loci (microsatellites) and immune genes (i.e., toll-like receptors) in an understorey bird species, the wedge-billed woodcreeper <i>Glyphorynchus spirurus</i>. The objectives were (1) to investigate forest fragmentation effects on population genetic diversity, (2) to disentangle the relative role of demography (genetic drift and migration) and selection, and (3) to assess whether immunogenetic patterns could be associated with variation of ectoparasite (i.e., ticks) pressures. Our results revealed an erosion of neutral genetic diversity and a substantial genetic differentiation among fragmented populations, resulting from a decrease in landscape connectivity and leading to the divergence of distinct genetic pools at a small spatial scale. Patterns of genetic diversity observed for TLR4 and TLR5 were concordant with neutral genetic patterns, whereas those observed for TLR3 and TLR21 were discordant. This result underlines that the dominant evolutionary force shaping immunogenetic diversity (genetic drift vs. selection) may be different depending on loci considered. Finally, tick prevalence was higher in fragmented environments. We discussed the hypothesis that pathogen selective pressures may contribute to maintain adaptive genetic diversity despite the negative demographic effect of habitat fragmentation on neutral genetic diversity.</p>
Data from: Vaginal host immune-microbiome interactions in a cohort of primarily African-American women who ultimately underwent spontaneous preterm birth or delivered at term
<p><strong>Background</strong>: Recent studies suggest that alterations in the vaginal microbiome allow for the assessment of the risk for spontaneous preterm birth (PTB), the leading cause of neonatal morbidity and mortality worldwide. However, the associations between the local immune response and the vaginal microbiome are still poorly understood. Herein, we characterize the vaginal host immune-microbiome interactions in women who ultimately underwent PTB and in those who delivered at term.</p> <p><strong>Methods</strong>: Vaginal fluid samples from 52 pregnant women (of whom 18 underwent PTB and 34 delivered at term) were collected from 10-32 weeks in a case-control study. Concentrations of 33 immune mediators were determined using sensitive and specific immunoassays. The previously published 16S rRNA gene sequence and bacterial phylotype data of these subjects were utilized in this study. Linear mixed effects models were utilized to test associations between vaginal immune mediator concentrations and bacterial phylotype relative abundances.</p> <p><strong>Results</strong>: 1) Specific immune mediators (β-defensins 2 and 3, IL-1β, CXCL10, CCL2, CCL3, SLPI, and VEGF) correlated with 18 different vaginal bacterial phylotypes in the overall study population; 2) vaginal concentrations of CXCL10, CCL2, CCL3, SLP1 and VEGF negatively correlated with non-Lactobacillus members of the vaginal microbiome; 3) vaginal concentrations of CXCL10 were negatively correlated with 15 bacterial phylotypes, most of which are typical members of Community State Type IV of the vaginal microbiome, such as Gardnerella vaginalis, Megasphaera sp. type 1, and Atopobium vaginae; 4) Gemella spp. were negatively correlated with vaginal concentrations of VEGF, CCL2, CCL3, SLPI, and CXCL10; 5) when comparing PTB cases to term controls, five soluble immune mediators (CCL26, CCL22 and CCL2, CXCL10 and IL-16), and especially CCL26, were negatively correlated with five typical members of Community State Type IV: Sneathia sanguinegens, Parvimonas micra, Veillonellaceae, BVAB2, and Gemella spp; and 6) Sneathia sanguinegens had stronger negative associations with all five soluble immune mediators (CCL26, CCL22 and CCL2, CXCL10 and IL-16) in PTB cases than in term controls.</p> <p><strong>Conclusions</strong>: The assessment of vaginal host immune-microbiome interactions revealed that specific soluble immune mediators, mainly CXCL10, negatively correlated with typical members of Community State Type IV of the vaginal microbiome. In addition, this assessment particularly showed that Sneathia sanguinegens had stronger negative associations with different immune mediators, including CXCL10 and CCL26, in women who ultimately had a PTB compared to those who delivered at term. These findings provide insight into the vaginal host immune-microbiome interactions in normal and complicated pregnancies.</p>
Male and female genotype and a genotype-by-genotype interaction mediate the effects of mating on cellular but not humoral immunity in female decorated crickets
<p>Sexually antagonistic coevolution is predicted to lead to the divergence of male and female genotypes related to the effects of substances transferred by males at mating on female physiology. The outcome of mating should thus depend on the specific combination of mating genotypes. Although mating has been shown to influence female immunity in diverse insect taxa, a male-female genotype-by-genotype effect on female immunity post-mating remains largely unexplored. Here, we investigate the effects of mating on female decorated cricket baseline immunity and the potential for a male-by-female genotype interaction affecting this response. Females from three distinct genotypic backgrounds were left unmated or singly mated in a fully reciprocal design to males from the same three genotypic backgrounds. Hemocytes and hemocyte microaggregations were quantified for female cellular immunity, and phenoloxidase, involved in melanization, and antibacterial activity for humoral immunity. In this system, female cellular immunity was more reactive to mating, and mating effects were genotype dependent. Specifically, for hemocytes, a genotype-mating status interaction mediated the effect of mating per se, and a significant male-female genotype-by-genotype interaction determined hemocyte depletion post-mating. Microaggregations were influenced by the female's genotype or that of her mate. Female humoral immune measures were unaffected, indicating the propensity for post-mating effects on female is dependent on the component of baseline immunity. The genotype-by-genotype effect on hemocytes supports a role of sexual conflict in post-mating immune suppression, suggesting divergence of male genotypes with respect to modification of female post-mating immunity, and divergence of female genotypes in resistance to these effects.</p>
Human genomics of the humoral immune response against polyomaviruses
<p>Meta-analyses results of the manuscript "Human genomics of the humoral immune response against polyomaviruses".</p>
Innate immunity promotes sleep through epidermal antimicrobial peptides
<p>Wounding and infection trigger a protective innate immune response that includes the production of antimicrobial peptides in the affected tissue as well as increased sleep. Little is known, however, how peripheral wounds or innate immunity signal to the nervous system to increase sleep. We found that during <i>C. elegans</i> larval molting, an epidermal tolloid/BMP-1-like protein called NAS-38 promotes sleep. NAS-38 is negatively regulated by its thrombospondin domain and acts through its astacin protease domain to activate p38 MAP/PMK-1 kinase and TGF-β-SMAD/SMA-3-dependent innate immune pathways in the epidermis that cause STAT/STA-2 and SLC6 (solute carrier)/SNF-12-dependent expression of antimicrobial peptide (AMP) genes. We show that more than a dozen epidermal AMPs act as somnogens, signaling across tissues to promote sleep through the sleep-active RIS neuron. In the adult, epidermal injury activates innate immunity and turns up AMP production to trigger sleep, a process that requires EGFR signaling that is known to promote sleep following cellular stress. We show for one AMP, NLP-29, that it acts through the neuropeptide receptor NPR-12 in locomotion-controlling neurons that are presynaptic to RIS and that depolarize this neuron to induce sleep. Sleep in turn increases the chance of surviving injury. Thus, we found a novel mechanism by which peripheral wounds signal to the nervous system to increase protective sleep. Such a cross-tissue somnogen signaling function of AMPs might also boost sleep in other animals including humans.</p>
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.