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12,799 results for “Immunization”
The translational landscape of SARS-CoV-2 and infected cells reveals suppression of innate immune genes
<p>SARS-CoV-2 utilizes a number of strategies to modulate viral and host mRNA translation. Here, we used ribosome profiling in SARS-CoV-2 infected model cell lines and primary airway cells grown at the air-liquid interface to gain a deeper understanding of the translationally regulated events in response to virus replication. We find that SARS-CoV-2 mRNAs dominate the cellular mRNA pool but are not more efficiently translated than cellular mRNAs. SARS-CoV-2 utilized a highly efficient ribosomal frameshifting strategy despite notable accumulation of ribosomes within the slippery sequence on the frameshifting element. In the highly permissive cell models, although SARS-CoV-2 infection induced the transcriptional upregulation of numerous chemokines, cytokines and interferon stimulated genes, many of these mRNAs were not translated efficiently. Impact of SARS-CoV-2 on host mRNA translation was more subtle in primary cells, with marked transcriptional and translational upregulation of inflammatory and innate immune responses and downregulation of processes involved in ciliated cell function. Together, these data reveal the key role of mRNA translation in SARS-CoV-2 replication and highlight unique mechanisms for therapeutic development. The processed data presented here is derived from the relevant RNA-seq and ribo-seq libraries.</p>
Genetic and immunological evaluation of children with inborn errors of immunity and hypoxemic COVID-19 pneumonia
<p><strong><em>Background:</em></strong> SARS-CoV-2 has infected more than 450 million people around the world. In about 10% of cases, the infection leads to hypoxemic pneumonia, which is much rarer in children, while multisystem inflammation is seen almost only in children.</p> <p><strong><em>Methods:</em></strong> We evluated 31 young patients (0.5-19 years) who had both pre-existing inborn errors of immunity (IEI) and were later diagnosed with COVID-19 complications. Whole-exome sequencing was performed, SARS-CoV-2 specific antibodies and autoantibody against type I interferons were measured and plasma inflammatory factors were profiled. We also reviewed COVID-19 disease severity and outcome in IEI patients in the literature.</p> <p><strong><em>Results:</em></strong> A potential genetic cause of the IEI was identified in 28 patients (90.3%). The IgM and IgG-specific antibody response against the spike protein of the virus was positive in 14 (66.6%) of the IEI patients tested. Autoantibodies neutralizing type I interferons were identified in the plasma of two patients (6.8% of tested samples). Five patients fulfilled the diagnostic criteria of multisystem inflammatory syndrome in children (MIS-C). Eleven patients (35.4%) died due to COVID-19 complications showing a 3000 fold higher mortality rate compared to normal COVID-19 death rate in children (0.01%). For the additional 696 IEI patients reported till date, severe presentation of COVID-19 was observed in 23.3% of cases. Furthermore, a 5-fold higher mortality rate was observed, when compared with global infection-fatality reports.</p> <p><strong><em>Conclusions:</em></strong> Elucidating the genetic basis of IEI patients with severe/critical COVID-19 may help to better understand the human innate and adaptive immune response against SARS-CoV-2, which may assist to develop better preventive and therapeutic strategies.</p>
The developmental high-wire: Balancing resource investment in immunity and reproduction
<p>The strategic allocation of resources into immunity poses a unique challenge for individuals, where infection at different stages of development may result in unique trade-offs with concurrent physiological processes or future fitness-enhancing traits. Here, we experimentally induced an immune challenge in female <em>Gryllus firmus</em> crickets to test whether illness at discrete life stages differentially impacts fitness. We injected heat-killed <em>Serratia marcescens</em> bacteria into antepenultimate juveniles, penultimate juveniles, sexually-immature adults, and sexually-mature adults, and then measured body growth, instar duration, mating rate, viability of stored sperm, egg production, oviposition rate, and egg viability. Immune activation significantly impacted reproductive traits, where females that were immune-challenged as adults had decreased mating success and decreased egg viability compared to healthy individuals or females that were immune-challenged as juveniles. Although there was no effect of an immune challenge on the other traits measured, the stress of handling resulted in reduced mass gain and smaller adult body size in females from the juvenile treatments, and females in the adult treatments suffered from reduced viability of sperm stored within their spermatheca. In summary, we found that an immune challenge does have negative impacts on reproduction, but also that even minor acute stressors can have significant impacts on fitness-enhancing traits. These findings highlight that the factors affecting fitness can be complex and at times unpredictable, and that the consequences of illness are specific to when during an individual's life an immune-challenge is induced.</p>
Raw data for the study titled "Fungal ectoparasites increase winter mortality of ladybird hosts despite limited effects on their immune system"
<p>Winter represents a challenging period for insects inhabiting temperate regions. A plethora of studies have investigated how abiotic environmental conditions such as temperature affect insect overwintering success. However, only a few studies have focused on biotic factors and the mechanisms affecting the overwintering performance of insects. Here, we investigated the effects of the parasitic fungus <em>Hesperomyces virescens</em> on the overwintering performance and immune system functioning of the invasive ladybird <em>Harmonia axyridis</em>. Winter survival was significantly lower for infected than for uninfected beetles. Body mass loss during overwintering tend to be higher for infected individuals compared to uninfected ones and for larger beetles. In addition, parasitic infection reduced post-winter longevity without food in male but not female ladybirds. Total haemocyte and protein concentration as well as antimicrobial activity against <em>Escherichia coli</em> significantly decreased during ladybird overwintering. However, haemolymph parameters were only poorly affected by <em>Hesperomyces</em> infection, with the exception of antimicrobial activity against <em>Escherichia coli</em> that tended to be higher in infected ladybirds. Interestingly, none of the pre-winter haemolymph parameters were good predictors of ladybird winter survival. Overall, our results indicate that energy exhaustion unrelated to immune system challenge is the most probable explanation for increased overwintering mortality in infected beetles.</p>
Single Cell Profiling of Human Dura and Meningioma Reveals Cellular Meningeal Landscape and Insights into Meningioma Immune Response
<p>This repository contains the single-cell RNA-seq data described in the publication “Single Cell Profiling of Human Dura and Meningioma Reveals Cellular Meningeal Landscape and Insights into Meningioma Immune Response.” Data is provided as count matrices and Seurat objects.</p>
Consuming sunflower pollen reduced pathogen infection but did not alter measures of immunity in bumble bees
<p>Certain diets can benefit bee health by reducing pathogens, but the mechanism(s) driving these medicinal effects are largely unexplored. Recent research found that sunflower (<em>Helianthus annuus</em>) pollen reduces the gut pathogen <em>Crithidia bombi</em> in the common eastern bumble bee (<em>Bombus impatiens</em>). Here, we tested the effects of sunflower pollen and infection on two bee immune metrics to determine if sunflower pollen diet drives changes in host immunity that can explain this medicinal effect. Bees were infected with <em>C. bombi </em>or not and given either sunflower or wildflower pollen. Subsequently, bees received a benign immune challenge or were left naïve to test the induced and constitutive immune responses, respectively. We measured hemolymph phenoloxidase activity, involved in the melanization cascade, and antibacterial activity. Sunflower pollen reduced <em>C. bombi</em> infection, but we found no significant pollen diet effect on either immune measure. Phenoloxidase activity was also not affected by <em>C. bombi</em> infection status; however, uninfected bees were more likely to have measurable constitutive antibacterial activity, while infected bees had higher induced antibacterial activity. Overall, we found that sunflower pollen does not significantly affect the immune responses we measured, suggesting that the mechanisms underlying its medicinal effect do not involve these bee immune parameters.</p>
Extricating human tumour immune alterations from tissue inflammation
<p>This is the pre-processed and cleaned RDS file that contains the main sc-RNAseq data (10x platform) from inflamed oral mucosal (OM) and head-and-neck squamous cell carcinoma (HNSCC) tissues used in this publication (https://www.nature.com/articles/s41586-022-04718-w). Script for processing and generating figures is uploaded on Github: https://github.com/MairFlo/Tumor_vs_Inflamed.</p> <p> </p> <p>Abstract:</p> <p>Immunotherapies have achieved remarkable successes in the treatment of cancer, but major challenges remain<sup><a href="https://www.nature.com/articles/s41586-022-04718-w#ref-CR1">1</a>,<a href="https://www.nature.com/articles/s41586-022-04718-w#ref-CR2">2</a></sup>. An inherent weakness of current treatment approaches is that therapeutically targeted pathways are not restricted to tumours, but are also found in other tissue microenvironments, complicating treatment<sup><a href="https://www.nature.com/articles/s41586-022-04718-w#ref-CR3">3</a>,<a href="https://www.nature.com/articles/s41586-022-04718-w#ref-CR4">4</a></sup>. Despite great efforts to define inflammatory processes in the tumour microenvironment, the understanding of tumour-unique immune alterations is limited by a knowledge gap regarding the immune cell populations in inflamed human tissues. Here, in an effort to identify such tumour-enriched immune alterations, we used complementary single-cell analysis approaches to interrogate the immune infiltrate in human head and neck squamous cell carcinomas and site-matched non-malignant, inflamed tissues. Our analysis revealed a large overlap in the composition and phenotype of immune cells in tumour and inflamed tissues. Computational analysis identified tumour-enriched immune cell interactions, one of which yields a large population of regulatory T (T<sub>reg</sub>) cells that is highly enriched in the tumour and uniquely identified among all haematopoietically-derived cells in blood and tissue by co-expression of ICOS and IL-1 receptor type 1 (IL1R1). We provide evidence that these intratumoural IL1R1<sup>+</sup> T<sub>reg</sub> cells had responded to antigen recently and demonstrate that they are clonally expanded with superior suppressive function compared with IL1R1<sup>−</sup> T<sub>reg</sub> cells. In addition to identifying extensive immunological congruence between inflamed tissues and tumours as well as tumour-specific changes with direct disease relevance, our work also provides a blueprint for extricating disease-specific changes from general inflammation-associated patterns.</p>
Data from: Early detection of cerebrovascular pathology and protective antiviral immunity by MRI
<p>Central nervous system (CNS) infections are a major cause of human morbidity and mortality worldwide. Even patients that survive CNS infections can have lasting neurological dysfunction resulting from immune and pathogen induced pathology. Developing approaches to noninvasively track pathology and immunity in the infected CNS is crucial for patient management and development of new therapeutics. Here, we develop novel MRI-based approaches to monitor virus-specific CD8+ T cells and their relationship to cerebrovascular pathology in the living brain. We studied a relevant murine model in which a neurotropic virus (vesicular stomatitis virus) was introduced intranasally and then entered the brain via olfactory sensory neurons – a route exploited by many pathogens in humans. Using T2*-weighted high-resolution MRI, we identified small cerebral microbleeds as the earliest form of pathology associated with viral entry into the brain. Mechanistically, these microbleeds occurred in the absence of peripheral immune cells and were associated with infection of vascular endothelial cells. We monitored the adaptive response to this infection by developing methods to iron label and track individual virus specific CD8+ T cells by MRI. Transferred antiviral T cells were detected in the brain within a day of infection and were able to reduce cerebral microbleeds. These data demonstrate the utility of MRI in detecting the earliest pathological events in the virally infected CNS as well as the therapeutic potential of antiviral T cells in mitigating this pathology.</p>
Seasonality of host immunity in a tropical disease system
<p>Infectious disease systems frequently exhibit strong seasonal patterns, yet the mechanisms that underpin intra-annual cycles are unclear, particularly in tropical regions. We hypothesized that host immune function fluctuates seasonally, contributing to oscillations in infection patterns in a tropical disease system. To test this hypothesis, we investigated a key host defense of amphibians against a lethal fungal pathogen, <em>Batrachochytrium dendrobatidis</em> (<em>Bd</em>). We integrated two field experiments in which we perturbed amphibian skin secretions, a critical host immune mechanism, in Panamanian rocket frogs (<em>Colostethus panamansis</em>). We found that this immunosuppressive technique of reducing skin secretions in wild frog populations increased <em>Bd</em> prevalence and infection intensity, indicating that this immune defense contributes to resistance to <em>Bd</em> in wild frog populations. We also found that the chemical composition and anti-<em>Bd</em> effectiveness of frog skin secretions varied across seasons, with greater pathogen inhibition during the dry season relative to the wet season. These results suggest that the effectiveness of this host defense mechanism shifts across seasons, likely contributing to seasonal infection patterns in a lethal disease system. More broadly, our findings indicate that host immune defenses can fluctuate across seasons, even in tropical regions where temperatures are relatively stable, which advances our understanding of intra-annual cycles of infectious disease dynamics.</p>
Data and code for the manuscript titled "Persistence of SARS-CoV-2 immunity, Omicron's footprints, and projections of epidemic resurgences in South African population cohorts"
<p>Data and code for the manuscript titled “Persistence of SARS-CoV-2 immunity, Omicron’s footprints, and projections of epidemic resurgences in South African population cohorts”</p>
Integration of single-cell RNA-sequencing data across tissues and cancer types towards immune cell characterization
<p>To better understand dendritic cell states and subtypes, we collected individual single-cell RNAseq datasets from various studies and further integrated, batch corrected, and reprocessed the data using Besca (https://github.com/bedapub/besca).</p> <p>The following files are included:<br> 1) study_table_integrated_DCs.xlsx - contains a list of studies from where the datasets were gathered.<br> 2) int_dcs.raw.h5ad - An anndata object file containing the combined raw single-cell counts for DCs from individual studies. The datasets were joined based on the union of variables.<br> 3) intersection_genes_integrated_dcs.tsv - List of genes if the datasets were joined based on the intersection of variables. These variables were used in the subsequent analyses.</p> <p>4) int_dcs.annotated.h5ad - An anndata object file containing single-cell logarithmized counts for DCs data that have been integrated and reprocessed. The rows of the file contain cells, and the columns contain highly variable genes. A sparse matrix containing the logarithmized counts from all the genes (from the intersection genes integrated dcs.tsv file) can also be found (adata.raw.X) in the object. In the observations, cell-type annotation is available at three different hierarchal levels.<br> <br> This data was further used to produce results for the publication (https://jitc.bmj.com/content/10/6/e004268) on the effects of Toll-like receptor 8 agonists on conventional DCs.</p>
Processed Seurat Object of scRNAseq data from wildtype and CaMKK2 KO immune infiltrate of CT2a preclinical murine glioma
<p>This repository contains the processed Seurat objects generated from the raw data deposited at the Gene Expression Omnibus (GEO) under GSE197879.</p> <p>Details about the experiment and sequencing are available under GSE197879.</p> <p>Information on how the Seurat objects were created can be found in this GitHub repository https://github.com/wht10/CT2A_scRNAseq_CaMKK2KOvWT .</p> <p>Notable metadata within each Seurat object:</p> <p>1. Processed_CD45_Live_Fig2b.rds</p> <ul> <li>Genotype - whether the cell is from a WT or CaMKK2 KO mouse</li> <li>HTO_maxID - The biological replicate that the cell came from (4 biological replicates per genotype)</li> <li>MouseID - A concatenation between the genotype and HTO_maxID, providing a unique identifier for each biological replicate</li> <li>Cell.Type - The cell type annotations for each cell. Can be assigned to "Idents()" to change the name of the cell identities.</li> <li>Geno.Ident - A concatenation between Genotype and Cell.Type. By re-assigning this to "Idents()" "FindMarkers()" can be used to investigate differentially expressed genes within a cell-type between genotypes. </li> </ul> <p>2. Reclustered_TILs_Fig3a.rds</p> <ul> <li>Genotype - whether the cell is from a WT or CaMKK2 KO mouse</li> <li>HTO_maxID - The biological replicate that the cell came from (4 biological replicates per genotype)</li> <li>MouseID - A concatenation between the genotype and HTO_maxID, providing a unique identifier for each biological replicate</li> <li>Celltype - The cell type annotations for each cell. Can be assigned to "Idents()" to change the name of the cell identities.</li> <li>Geno_Ident - A concatenation between Genotype and cell-type. By re-assigning this to "Idents()" "FindMarkers()" can be used to investigate differentially expressed genes within a cell-type between genotypes. </li> </ul>
Variations in immune parameters with age in a wild rodent population and links with survival
<p>Recent findings suggest that immune functions do not unidirectionally deteriorate with age but that a potentially adaptive remodelling, where functions of the immune system get down regulated while others get upregulated with age could also occur. Scarce in wild populations, longitudinal studies are yet necessary to properly understand the patterns and consequences of age variations of the immune system in the wild. Meanwhile, it is challenging to understand if the observed variations in immune parameters with age are due to changes at the within-individual level or to selective (dis)appearance of individuals with peculiar immune phenotypes. Thanks to a long-term and longitudinal monitoring of a wild Alpine marmot population, we aimed to understand within- and between-individual variation in the immune phenotype with age, in order to improve our knowledge about the occurrence and the evolutionary consequences of such age-variations in the wild. To do so, we recorded the age-specific leukocyte concentration and leukocyte profile in repeatedly sampled dominant individuals. We then tested whether the potential changes with age were attributable to within-individual variations and/or selective (dis)appearance. Finally, we investigated if the leukocyte concentration and profiles were correlated to the probability of death at a given age. The leukocyte concentration was stable with age, but the relative number of lymphocytes decreased, while the relative number of neutrophils increased, over the course of an individual's life. Moreover, between individuals of the same age, individuals with fewer lymphocytes but more neutrophils were more likely to die. Therefore, selective disappearance seems to play a role in the age variations of the immune parameters in this population. Further investigations linking age variations in immune phenotype to individual fitness are needed to understand whether remodelling of the immune system with age could or could not be adaptive.</p>
Humoral immunity of voles Cricetidae Rodentia in Siberia
<p><span>We studied the seasonal variation of adaptive humoral immunity (AHI) in northern red-backed vole (<em>Clethrionomys rutilus</em> Pallas, 1779, RBV) and grey-sided vole (<em>C. rufocanus</em></span> <span>Sundevall, 1846, GSV) in Tomsk region of Western Siberia. Immunoresponsiveness (IR) to sheep red blood cells was assessed by the number of antibody-producing cells in the spleen. The use of a generalized linear model to analyze the effects of species, sex, year of research, and season of withdrawal of individuals from nature on IR showed a significant effect of species identity, season of animals capture and the interaction of species with season. The RBV demonstrated higher immune responses during a year, and both species had higher IR in winter. Suppression of IR in spring was greater, started earlier and lasted longer (March–May) in GSV. In RBV, immunosuppression was restricted to April. The significant negative within year correlations of IR with body mass and masses of reproductive organs in GSV a tradeoff between AHI and growth and reproduction processes. A reason for the difference between species in the seasonal variation of AHI may be related to the difference in tropho-energetic requirements of each vole species. GSV is a predominantly herbivorous rodent and its thermoregulation seems less efficient than of RBV. The deeper spring immunosuppression in GSV may explain in part its higher mortality during the season of colds.</span></p>
Supplementary Tables: Host cellular immunity and nutrition respond to intracellular symbiont abundance in an obligate deep-sea symbiosis
<p>Contains supplementary tables for the pre-print manuscript: Host cellular immunity and nutrition respond to intracellular symbiont abundance in an obligate deep-sea symbiosis</p>
Spatially variant immune infiltration scoring in human cancer tissues
<p>IMC raw dataset for cohort 1 and cohort 2 for the paper: "Spatially variant immune infiltration scoring in human cancer tissues"</p>
Immune parameters in horses under different housing conditions - revised version
<p>Horses were successively subjected to two different treatments - 1. fission of a stable group, 2. relocation to single housing - and the blood numbers of various leukocytes subsets invesigated. In addition, plasma cortisol concentrations, individual rank, and number of social interactions before and after fission of the group as well as occurrence of stereotypic behavior after relocation to individual stabling was assessed.</p>
Immune responses in mice lacking STAT-1 in microglia
<p><em>Toxoplasma gondii</em> is a ubiquitous intracellular protozoan parasite that establishes a life-long chronic infection largely restricted to the central nervous system (CNS). Constant immune pressure, notably IFN-γ-STAT1 signaling, is required for preventing fatal pathology during <em>T. gondii</em> infection. Here, we report that abrogation of STAT1 signaling in microglia, the resident immune cells of the CNS, is sufficient to induce a loss of parasite control in the CNS and susceptibility to toxoplasmic encephalitis during the early stages of chronic infection. Using a microglia-specific genetic labeling and targeting system that discriminates microglia from blood-derived myeloid cells that infiltrate the brain during infection, we find that, contrary to previous in vitro reports, microglia do not express inducible nitric-oxide synthase (iNOS) during <em>T. gondii</em> infection in vivo. Instead, transcriptomic analyses of microglia reveal that STAT1 regulates both (i) a transcriptional shift from homeostatic to "disease-associated microglia" (DAM) phenotype conserved across several neuroinflammatory models, including <em>T. gondii</em> infection, and (ii) the expression of anti-parasitic cytosolic molecules that are required for eliminating T. gondii in a cell-intrinsic manner. Further, genetic deletion of Stat1 from microglia during T. gondii challenge leads to fatal pathology despite largely equivalent or enhanced immune effector functions displayed by brain-infiltrating immune populations. Finally, we show that microglial STAT1-deficiency results in the overrepresentation of the highly replicative, lytic tachyzoite form of <em>T. gondii</em>, relative to its quiescent, semi-dormant bradyzoite form typical of chronic CNS infection. Our data suggest an overall protective role of CNS-resident microglia against<em> T. gondii</em> infection, illuminating (i) general mechanisms of CNS-specific immunity to infection (ii) and a clear role for IFN-STAT1 signaling in regulating a microglial activation phenotype observed across diverse neuroinflammatory disease states.</p>
Immune signatures predict development of autoimmune toxicity in immune checkpoint inhibitor-treated patients with cancer
<p><strong>Immune signatures predict development of autoimmune toxicity in immune</strong><strong> checkpoint inhibitor-treated patients with cancer</strong></p> <p> </p> <p>Nicolas Gonzalo Nuñez<sup>1</sup>*, Fiamma Berner<sup>2</sup>*, Ekaterina Friebel<sup>1</sup>*, Susanne Unger<sup>1</sup>, Nina Wyss<sup>2,3</sup>, Julia Martinez Gomez<sup>4</sup>, Mette-Triin Purde<sup>2</sup>, Rebekka Niederer<sup>2,3</sup>, Maximilian Porsch<sup>5</sup>, Christa Lichtensteiger<sup>2</sup>, Rafaela Kramer<sup>6</sup>, Michael Erdmann<sup>6</sup>, Christina Schmitt<sup>7</sup>, Lucy Heinzerling<sup>6,7</sup>, Marie-Therese Abdou<sup>2</sup>, Julia Karbach<sup>8</sup>, Dirk Schadendorf<sup>9</sup>, Lisa Zimmer<sup>9</sup>, Selma Ugurel<sup>9</sup>, Niklas Klümper<sup>10,11,12</sup>, Michael Hölzel<sup>10,11</sup>, Laura Power<sup>1</sup>, Stefanie Kreutmair<sup>1</sup>, Mariaelena Capone<sup>13</sup>, Gabriele Madonna<sup>13</sup>, Lacin Cevhertas<sup>14,15</sup>, Anja Heider<sup>14</sup>, Teresa Amaral<sup>16,17</sup>, Omar Hasan Ali<sup>2,3,4,18</sup>, David Bomze<sup>2,19</sup>, Florentia Dimitriou<sup>4</sup>, Stefan Diem<sup>20</sup>, Paolo Antonio Ascierto<sup>13</sup>, Reinhard Dummer<sup>4</sup>, Elke Jäger<sup>8</sup>, Christoph Driessen<sup>20</sup>, Mitchell P. Levesque<sup>4</sup>, Willem van de Veen<sup>14</sup>, Markus Joerger<sup>20</sup>, Martin Früh<sup>20,21</sup>, Burkhard Becher<sup>1</sup>**, Lukas Flatz<sup>2,3,4,20,22</sup>**</p> <p> </p> <p>*/** these authors contributed equally</p> <p> Affiliations</p> <p>1. Institute of Experimental Immunology, University of Zurich, Zurich, Switzerland</p> <p>2. Institute of Immunobiology, Medical Research Center, Kantonsspital St. Gallen, St.Gallen, Switzerland</p> <p>3. Department of Dermatology, Kantonsspital St. Gallen, St.Gallen, Switzerland</p> <p>4. Department of Dermatology, University Hospital Zurich, Zurich, Switzerland</p> <p>5. Department of Radiology, Kantonsspital St. Gallen, St.Gallen, Switzerland</p> <p>6. Department of Dermatology, University of Erlangen-Nuremberg, Erlangen, Germany</p> <p>7. Ludwig Maximilian University of Munich, Munich, Germany</p> <p>8. Department of Oncology and Hematology, Krankenhaus Nordwest, Frankfurt, Germany</p> <p>9. Department of Dermatology, Comprehensive Cancer Center (Westdeutsches Tumorzentrum) University Hospital Essen, Essen, Germany</p> <p>10. Institute for Experimental Oncology, University Hospital Bonn, Bonn, Germany</p> <p>11. Center for Integrated Oncology Cologne/Bonn, University Hospital Bonn, Bonn, Germany</p> <p>12. Department of Urology, University Hospital Bonn, Bonn, Germany</p> <p>13. Istituto Nazionale Tumori-IRCCS-Fondazione G. Pascale, Napoli, Italy</p> <p>14. Swiss Institute of Allergy and Asthma Research (SIAF), University of Zurich, Davos, Switzerland</p> <p>15. Department of Medical Immunology, Institute of Health Sciences, Bursa Uludag University, Bursa, Turkey</p> <p>16. Skin Cancer Center, Department of Dermatology, University Hospital Tübingen, Tübingen, Germany</p> <p>17. iFIT Cluster of Excellence (EXC 2180), University of Tübingen, Tübingen, Germany</p> <p>18. Department of Medical Genetics, Life Sciences Institute, University of British Columbia, Vancouver, Canada</p> <p>19. Sackler Faculty of Medicine, Tel-Aviv University, Israel</p> <p>20. Department of Oncology, Kantonsspital St. Gallen, St.Gallen, Switzerland</p> <p>21. Department of Medical Oncology, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland</p> <p>22. Universitäts-Hautklinik, University of Tübingen, Tübingen, Germany</p> <p> </p> <p> </p>
Immune assay data for Lycaeides melissa larvae reared on different host plants and with/without egg microbes
<p class="MsoListParagraphCxSpFirst"><span>1.<span> </span></span><span>Maternally transmitted microbes are ubiquitous. In insects, maternal microbes can play a role in mediating the insect immune response. </span><span>Less is known about how ecological factors, such as resource use, interact with maternal microbes to affect immunity. </span></p> <p class="MsoListParagraphCxSpMiddle"><span>2.<span> </span></span><span>In the context of a recent colonization of a novel host plant by the Melissa blue butterfly (<em>Lycaeides melissa</em>), we investigated the interaction between host plant use and vertically transmitted, extracellular egg-associated microbes in determining the strength of the insect immune response. </span></p> <p class="MsoListParagraphCxSpMiddle"><span>3.<span> </span></span><span>We reared larvae on two different host plant species: a native host <em>Astragalus canadensis</em> and a novel host <em>Medicago sativa</em>. Egg-associated microbes were removed through a series of antimicrobial egg washes prior to hatching. Immune response was measured through three assays: standing phenoloxidase (PO), total PO, and melanization. </span></p> <p class="MsoListParagraphCxSpMiddle"><span>4.<span> </span></span><span>We detected strong effects of microbial removal. Egg washing resulted in larvae with an increased immune response as measured by total PO- contrary to reports from other taxa. The effect of washing was especially strong for larvae consuming the native host plant. </span></p> <p> </p> <p class="MsoListParagraphCxSpLast"><span>5.<span> </span></span><span>This result may explain why consumption of the egg casing is not a universal behaviour in insects, due to negative effects on larval immunity. </span></p>
ScienceDex guides
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
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.