Host pathways mediating changes in immune states elicited by intestinal microbial colonization are incompletely characterized. Here we describe alterations of the host immune state induced by colonization of germ-free zebrafish larvae with an intestinal microbial community or single bacterial species. We show that microbiota-induced changes in intestinal leukocyte subsets and whole-body host gene expression are dependent on the innate immune adaptor gene myd88. Similar patterns of gene expression are elicited by colonization with conventional microbiome, as well as mono-colonization with two different zebrafish commensal bacterial strains. By studying loss-of-function myd88 mutants, we find that colonization suppresses Myd88 at the mRNA level. Tlr2 is essential for microbiota-induced effects on myd88 transcription and intestinal immune cell composition. Overall design: Zebrafish embryos were sterilized to generate germ-free groups. Transcriptomic responses in germ-free embryos were were assessed relative to colonized embryos, either colonized by complex and in characterized microbial communities (Conventionalozation) or by specefic single commensal bacterial species (monoassociation, Exiguobacterium/Chryseobacterium)
Intestinal microbiome adjusts the innate immune setpoint during colonization through negative regulation of MyD88.
Treatment, Subject
View SamplesGene expression profiling of FACS sorted GFP+ve cells from sexed gonads of transgenic pSF1-eGFP mice
Expression profiling of purified mouse gonadal somatic cells during the critical time window of sex determination reveals novel candidate genes for human sexual dysgenesis syndromes.
No sample metadata fields
View SamplesIL-2 signals into CD8 T cells have a programming and regulatory role in driving cells to full effector and memory differentiation. This study was designed to look for IL-2 target genes that affect CD8 T cell responses.
Endoplasmic reticulum stress regulator XBP-1 contributes to effector CD8+ T cell differentiation during acute infection.
Sex, Specimen part
View SamplesFollowing infection with LCMV, CD4+ SMARTA TCR transgenic cells (specific for the gp61-80 epitope of the LCMV glycoprotein) rapidly expand, become effector cells, and go on to form a long-lived memory population. Following infection with a recombinant Listeria monocytogenes expressing the LCMV epitope gp61-80, SMARTA cells also expand but display defective effector differentiation and fail to form memory. In an attempt to understand the signals required for CD4 T cell memory differentiation, we compared gene expression by SMARTA cells at the peak of the primary response following either Lm-gp61 or LCMV infection.
Rapid culling of the CD4+ T cell repertoire in the transition from effector to memory.
No sample metadata fields
View SamplesWe noticed that ThPOK repression is readily abrogated upon in vitro TCR stimulation of peripheral CD8 T cells. This observation prompted us to investigate a role of ThPOK in the CD8 T cell response to an acute viral infection. We observed that clonal expansion is significantly less in both primary and secondary CD8 T cell responses in the absence of functional ThPOK. To approach this mechanism, we carried out a microarray analysis for comparison of gene expression between ThPOKhd/hd and ThPOKwt/wt P14 memory T cells.
ThPOK derepression is required for robust CD8 T cell responses to viral infection.
No sample metadata fields
View SamplesTissue resident memory (Trm) represent a newly described memory T cell population. We have previously characterized a population of Trm that persists within the brain following acute virus infection. Although capable of providing marked protection against a subsequent local challenge, brain Trm do not undergo recall expansion following dissociation from the tissue. Furthermore, these Trm do not depend on the same survival factors as the circulating memory T cell pool as assessed either in vivo or in vitro. To gain greater insight into this population of cells we compared the gene-expression profiles of Trm isolated from the brain to circulating memory T cells isolated from the spleen following an acute virus infection. Trm displayed altered expression of genes involved in chemotaxis, expressed a distinct set of transcription factors and overexpressed several inhibitory receptors. Cumulatively, these data indicates that Trm are a distinct memory T cell population disconnected from the circulating memory T cell pool and displaying a unique molecular signature which likely results in optimal survival and function within their local environment.
The molecular signature of tissue resident memory CD8 T cells isolated from the brain.
Specimen part
View SamplesThe aim of the experiment is to determine sugar and ABA responsive gene expression in Arabidopsis.
Establishing glucose- and ABA-regulated transcription networks in Arabidopsis by microarray analysis and promoter classification using a Relevance Vector Machine.
Age, Time
View SamplesThe pretreatment karyotype of leukemic blasts is currently the key determinant in therapy decision-making in acute myeloid leukemia (AML). However, approximately fifty percent of AML patients, often carrying a normal karyotype, are currently unclassifiable based these established methods. Gene expression profiling has proven to be valuable for risk stratification of AML.
Prediction of molecular subtypes in acute myeloid leukemia based on gene expression profiling.
Sex, Age, Specimen part, Disease, Disease stage
View SamplesMost organisms have an endogenous circadian clock that is synchronized to environmental signals such as light and temperature. Although circadian rhythms have been described in the nematode C. elegans at the behavioral level, these rhythms appear to be relatively non-robust. Moreover, in contrast to other animal models, no circadian transcriptional rhythms have been identified. Thus, whether this simple nematode contains a bona fide circadian clock remains an open question.
Genome-wide analysis of light- and temperature-entrained circadian transcripts in Caenorhabditis elegans.
Specimen part, Time
View SamplesBACKGROUND: Dietary ABA-supplementation modulates immune and inflammatory responses in mouse models of chronic and infectious disease. However, the underlying mechanisms by which ABA elicits its immune modulatory effects are not well understood. This project used a systems approach in combination with functional and in vivo studies to investigate the target gene pathways modulated by ABA in the context of an inflammatory LPS challenge.
Abscisic acid regulates inflammation via ligand-binding domain-independent activation of peroxisome proliferator-activated receptor gamma.
No sample metadata fields
View Samples