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Mitochondrial genome variation affects humoral and cell-mediated innate immune responses and infection outcomes

ABSTRACT: Mitochondrial genome variation affects humoral and cell-mediated innate immune responses and infection outcomes

PROVIDER: PRJNA1084779 | ENA |

REPOSITORIES: ENA

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Mitochondrial genome variation affects humoral and cell-mediated innate immune responses and infection outcomes

Project description:The role of mitochondria in both adaptive and innate immune responses is increasingly recognized, but the role of natural mitochondrial DNA (mtDNA) variation as an immunomodulatory factor has received less attention. One reason for this is the difficulty of separating the effect of mtDNA from that of the nuclear genome. By utilizing the fruit fly Drosophila melanogaster, a powerful model system, we created cytoplasmic hybrids, aka. cybrid lines, where unique mtDNAs (mitotypes) were introgressed into a controlled isogenic nuclear background. We harnessed a panel of cybrid lines to study the effect of mtDNA variation on humoral and cell-mediated innate immune responses. Mitotypes exhibited heterogeneity in infection outcomes upon bacterial, viral and parasitoid infections. One mitotype of note, mtKSA2 appeared to be more immunocompetent when compared to other mitotypes. We performed transcriptomic profiling of uninfected flies and flies infected with bacteria or a virus and compared them to a different mitotype in the same nuclear background to find the mechanistic basis of the immunocompetence. We found that mtKSA2 caused an upregulation of TCA and OXPHOS related genes and a downregulation of a multiple genes encoding for antimicrobial peptides in uninfected flies. Upon infection, mtKSA2 flies produced unique transcriptomes that were separated by infection type and duration. When we examined immune cells (hemocytes) in mtKSA2 larvae, we noted an increase in hemocyte numbers. These hemocytes were activated in the absence of infection, increased their production of ROS, and showed evidence of increased encapsulation efficiency upon parasitoid wasp infection. Overall, our results show that mtDNA variation acts as an immunomodulatory factor in both humoral and cell-mediated innate immunity and that specific mitotypes provide enhanced protection against infections.

2024-03-09 | GSE260986 | GEO

Innate gene signature distinguishes humoral versus cytotoxic responses to influenza vaccination

Project description:Whole blood transcriptomics analysis of healthy individuals, immunized with the trivalent 2012-2013 season flu vaccine via transcutaneous, intramuscular or intradermal route. We define an early gene expression profile, detected at day 1 after immunization, that is associated with the development of either humoral or cytotoxic CD8 T cell responses. We used System Biology approach to analyse vaccine efficacy in order to find innate predictive biomarkers of the quality of adaptive responses for potential clinical use in the future. Moreover, from a methodological point of view this study increases knowledges on how vaccine route(s) can affect resulting immune responses and into mechanisms involved in the induction of humoral and cellular immunity to influenza vaccination.

2019-07-01 | E-MTAB-7741 | biostudies-arrayexpress

Rhipicephalus microplushemocyte innate cellular and humoral immune responses to babesialinfection

Project description:Rhipicephalus microplushemocyte innate cellular and humoral immune responses to babesialinfection

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Low incubation temperature during early development negatively affects survival and related innate immune processes in zebrafish larvae exposed to lipopolysaccharide

Project description:Low incubation temperature during early development negatively affects survival and related innate immune processes in zebrafish larvae exposed to lipopolysaccharide

2018-12-31 | GSE104639 | GEO

Mechanism of cellular and humoral rejection

Project description:This study used RNAseq to study the mechanism of cellular and humoral rejection by comparing clinical samples of cellular, humoral, mixed, and normal.

2018-10-16 | GSE74261 | GEO

Regulation of the BCR signalosome by the class II peptide editor, H2-M, affects the development and repertoire of innate-like B cells

Project description:Immunopeptidome analysis from WT and H2M-KO mice using M5/114, 15G4 and KH74 antibody were analyzed. Details are published in the paper "Regulation of the BCR signalosome by the class II peptide editor, H2-M, affects the development and repertoire of innate-like B cells".

2021-11-29 | MSV000088470 | MassIVE

Prior vaccination exceeds prior infection in eliciting innate and humoral immune responses in Omicron infected outpatients

Project description:Prior vaccination exceeds prior infection in eliciting innate and humoral immune responses in Omicron infected outpatients

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Cis-regulatory variation affects gene expression dynamics

Project description:Cis-regulatory variation affects gene expression dynamics

| PRJNA695016 | ENA

IL-6-mediated endothelial injury impairs anti-viral humoral immunity

Project description:Endothelial function and integrity are compromised after allogeneic bone marrow transplantation (BMT) but how this affects immune responses broadly remains unknown. Using a preclinical model of cytomegalovirus (CMV) reactivation after BMT, we found compromised antiviral humoral responses induced by IL-6 signaling. IL-6 signaling in T cells maintained Th1 cells resulting in sustained IFN secretion which promoted endothelial cell (EC) injury, loss of the neonatal Fc receptor (FcRn) responsible for immunoglobulin G (IgG) recycling, and rapid IgG loss. In contrast, recipient IgG producing cells are rapidly eliminated after BMT. T cell-specific deletion of IL-6R led to persistence of recipient-derived CMV-specific IgG and inhibited CMV reactivation. Deletion of IFN in donor T cells also eliminated EC injury and FcRn loss. In a phase III clinical trial, blockade of IL-6R with tocilizumab promoted CMV-specific IgG persistence and significantly attenuated early HCMV reactivation. In sum, IL-6 invokes IFN-dependent EC injury and consequent IgG loss leading to CMV reactivation. Hence, cytokine inhibition represents a logical strategy to prevent endothelial injury thereby preserving humoral immunity after immunotherapy.

2024-04-01 | GSE252180 | GEO

Impact of Hells loss-of-function on DNA methylation in B cells during humoral immune responses: kinetic comparison of Mb1-Hells knockout and control mice by enzymatic-methyl sequencing

Project description:We are interested in deciphering the mechanism by which DNA methylation in late B cell differentiation affects humoral immune response. We were using enzymatic-methyl sequencing (EM-seq) and chose to study a very rare immunodeficiency called ICF type 4, where a point mutation in a gene encoding the protein HELLS causes a lack of both circulating antibodies and memory B cells in human. HELLS is a chromatin remodeler, that allows for DNA methylation to occur.

2023-07-27 | E-MTAB-12609 | biostudies-arrayexpress

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