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      Intestinal transcriptomes in Kazakh sheep with different haplotypes after experimental Echinococcus granulosus infection Translated title: Transcriptomes intestinaux chez des moutons kazakhs de différents haplotypes après une infection expérimentale avec Echinococcus granulosus

      1 , 2 , 2 , 2 , 2 , *

      Parasite

      EDP Sciences

      Differentially expressed genes, Disease resistance, Echinococcus granulosus, Intestinal tissue, Transcriptome analysis

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          Abstract

          Cystic echinococcosis (CE) is a chronic zoonosis caused by infection with the larval stage of the cestode Echinococcus granulosus. As the intermediate host, sheep are highly susceptible to this disease. Our previous studies have shown that sheep with haplotype MHC Mva Ibc- Sac IIab- Hin1I ab were resistant to CE infection, while their counterparts without this haplotype were not. In order to reveal the molecular mechanism of resistance in Kazakh sheep, after selecting the differential miRNA in our previous study, herein, transcriptome analyses were conducted to detect the differential expression genes in the intestinal tissue of Kazakh sheep with resistant and non-resistant MHC haplotypes, after peroral infection with E. granulosus eggs. A total of 3835 differentially expressed genes were identified between the two groups, with 2229 upregulated and 1606 downregulated. Further function analysis showed that the most significant genes were related to both innate immune response and adaptive response participating in the defense against E. granulosus infection and the metabolic changes associated with it. The results suggest that genes related to lectin receptors, NK cells activation, chemokines, and tumor necrosis factor, may play important roles in the response of intestinal tissue to E. granulosus.

          Translated abstract

          L’échinococcose kystique (EK) est une zoonose chronique qui est causée par une infection au stade larvaire du cestode Echinococcus granulosus. En tant qu’hôte intermédiaire, les moutons sont très sensibles à cette maladie. Nos études précédentes ont montré que les moutons avec l’haplotype MHC Mva Ibc-Sac IIab-Hin1I ab étaient résistants à l’EK, alors que leurs homologues sans cet haplotype ne l’étaient pas. Afin de révéler le mécanisme moléculaire de la résistance chez le mouton kazakh, après avoir sélectionné le miARN différentiel dans notre étude précédente, des analyses de transcriptome ont été menées dans ce travail pour détecter les gènes d’expression différentielle dans le tissu intestinal de mouton kazakh avec des haplotypes MHC résistants et non résistants, après une infection pérorale par des œufs d’ E. granulosus. Un total de 3835 gènes différentiellement exprimés ont été identifiés entre les deux groupes, avec 2229 régulés à la hausse et 1606 à la baisse. Une analyse fonctionnelle plus poussée a montré que les gènes les plus significatifs étaient liés à la fois à la réponse immunitaire innée et à la réponse adaptative participant à la défense contre l’infection à E. granulosus et aux changements métaboliques qui y étaient associés. Les résultats suggèrent que les gènes liés aux récepteurs de la lectine, à l’activation des cellules NK, aux chimiokines et au facteur de nécrose tumorale peuvent jouer un rôle important dans la réponse du tissu intestinal à E. granulosus.

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          Most cited references 56

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          Activation of NK cells and T cells by NKG2D, a receptor for stress-inducible MICA.

          Stress-inducible MICA, a distant homolog of major histocompatibility complex (MHC) class I, functions as an antigen for gammadelta T cells and is frequently expressed in epithelial tumors. A receptor for MICA was detected on most gammadelta T cells, CD8+ alphabeta T cells, and natural killer (NK) cells and was identified as NKG2D. Effector cells from all these subsets could be stimulated by ligation of NKG2D. Engagement of NKG2D activated cytolytic responses of gammadelta T cells and NK cells against transfectants and epithelial tumor cells expressing MICA. These results define an activating immunoreceptor-MHC ligand interaction that may promote antitumor NK and T cell responses.
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            Mapping and quantifying mammalian transcriptomes by RNA-Seq.

            We have mapped and quantified mouse transcriptomes by deeply sequencing them and recording how frequently each gene is represented in the sequence sample (RNA-Seq). This provides a digital measure of the presence and prevalence of transcripts from known and previously unknown genes. We report reference measurements composed of 41-52 million mapped 25-base-pair reads for poly(A)-selected RNA from adult mouse brain, liver and skeletal muscle tissues. We used RNA standards to quantify transcript prevalence and to test the linear range of transcript detection, which spanned five orders of magnitude. Although >90% of uniquely mapped reads fell within known exons, the remaining data suggest new and revised gene models, including changed or additional promoters, exons and 3' untranscribed regions, as well as new candidate microRNA precursors. RNA splice events, which are not readily measured by standard gene expression microarray or serial analysis of gene expression methods, were detected directly by mapping splice-crossing sequence reads. We observed 1.45 x 10(5) distinct splices, and alternative splices were prominent, with 3,500 different genes expressing one or more alternate internal splices.
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              Signalling through C-type lectin receptors: shaping immune responses

              Key Points Crosstalk between pattern recognition receptors (PRRs) expressed by dendritic cells orchestrates T helper (TH) cell differentiation through the induction of specific cytokine expression profiles, tailored to invading pathogens. C-type lectin receptors (CLRs) have an important role in orchestrating the induction of signalling pathways that regulate adaptive immune responses. CLRs can control adaptive immunity at various levels by inducing signalling on their own, through crosstalk with other PRRs or by inducing carbohydrate-specific signalling pathways. DC-specific ICAM3-grabbing non-integrin (DC-SIGN) interacts with mannose-carrying pathogens including Mycobacterium tuberculosis, HIV-1, measles virus and Candida albicans to activate the serine/threonine protein kinase RAF1. RAF1 signalling leads to the acetylation of Toll-like receptor (TLR)-activated nuclear factor-κB (NF-κB) subunit p65 and affects cytokine expression, such as inducing the upregulation of interleukin-10 (IL-10). DC-associated C-type lectin 1 (dectin 1) triggering by a broad range of fungal pathogens, such as C. albicans, Aspergillus fumigatus and Pneumocystis carinii, results in protective antifungal immunity through the crosstalk of two independent signalling pathways — one through spleen tyrosine kinase (SYK) and one through RAF1 — that are essential for the expression of TH1 and TH17 cell polarizing cytokines. Crosstalk between the SYK and RAF1 pathways is both synergistic and antagonizing to fine-tune NF-κB activity: although Ser276 phosphorylation of p65 leads to enhanced transcriptional activity of p65 itself through acetylation, it also inhibits the transcriptional activity of the NF-κB subunit RELB by sequestering it in p65–RELB dimers, which are transcriptionally inactive. The diversity in CLR-mediated signalling provides some major challenges for the researches to elucidate and manipulate the signalling properties of this exciting family of receptors. However, the recent advances strongly support the use of CLR targeting vaccination strategies using dendritic cells to induce or redirect adaptive immune responses as well as improve antigen delivery.
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                Author and article information

                Journal
                Parasite
                Parasite
                parasite
                Parasite
                EDP Sciences
                1252-607X
                1776-1042
                2021
                05 March 2021
                : 28
                : ( publisher-idID: parasite/2021/01 )
                Affiliations
                [1 ] College of Life Sciences, Shihezi University Road Beisi Shihezi 832003 Xinjiang PR China
                [2 ] College of Animal Science and Technology, Shihezi University Road Beisi Shihezi 832003 Xinjiang PR China
                Author notes
                [a]

                Institutes 1 and 2 contributed equally.

                [* ]Corresponding author: 215273439@ 123456qq.com
                Article
                parasite200166 10.1051/parasite/2021011
                10.1051/parasite/2021011
                7934610
                33666549
                © X. Li et al., published by EDP Sciences, 2021

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Page count
                Figures: 4, Tables: 3, Equations: 0, References: 51, Pages: 11
                Categories
                Research Article

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