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The endoplasmic reticulum (ER) is considered as an essential eukaryotic organelle because of its role in the quality control of secreted proteins. However, there are situations that can lead to the development of the endoplasmic reticulum stress through the activation of an enzyme called “c-Jun N-terminal Kinases” (JNK), and this participate to the development of the insulin resistance. Indeed, the JNK is a kinase that phosphorylates serine residues of IRS-1 (Insulin receptor substrate-1), thereby blocking insulin receptor signalling. Furthermore, obesity leads to the development of the insulin resistance. Numerous studies have shown that the accumulation of fat mass is associated with a low-grade inflammatory state. Hence, the fat tissues secrete pro inflammatory cytokines such as TNFα. These cytokines can activate the JNK. Studies have shown that during the development of obesity, fat is infiltrated by macrophages and is responsible for the quasi totality of the TNFα secreted. Chronic insulin resistance state may cause type II diabetes. To improve insulin sensitivity, several possibilities were envisaged as the use of chaperon, or the loss of weight, but, the best treatment is the prevention, which consists in having a regular physical activity and in eating varied and balanced Le réticulum endoplasmique est u organiste essentiel aux eucaryotes car il exerce un véritable contrôle de qualité des protéines secrétées. Toutefois, certaines conditions peuvent mener au stress du réticulum et conduire au développement d’une insulino-résistance via l’activation d’une enzyme appelée « c-Jun N-terminal Kinase » (JNK). En effet, la JNK induit une phosphorylation des résidus sérines d’IRS-1 (Insulin receptor substrate 1), ce qui va provoquer une altération de la signalisation du récepteur à l’insuline. De plus, l’obésité favorise le développement de l’insulino-résistance. En effet, plusieurs études ont démontré que l’accumulation de masse grasse était liée à un été inflammatoire du tissu adipeux se traduisant notamment par une augmentation des taux de cytokines pro-inflammatoire telles que le Tumor Necrosis Factor-α (TNFα). Ces cytokine sauront pour effet d’induire l’activation de la JNK. D’autres études ont mis en évidence, qu’au cours de l’obésité, le tissu adipeux était infiltré par des macrophages et que ceux-ci seraient responsables de la quasi-totalité du TNFα secrété. Une insulino-résistance chronique peut mener à l’apparition du diabète de type II. Pour améliorer la sensibilité à l’insuline, plusieurs possibilités ont été envisagées comme l’utilisation des chaperonnes, ou la perte de poids, mais le meilleur traitement, reste la prévention, qui consiste à avoir une activité physique régulière et à manger varié et équilibré

Endoplasmic Reticulum Stress --- JNK Mitogen-Activated Protein Kinases --- Diabetes Mellitus, Type 2

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Unfolded protein response (UPR) is a cellular adaptive response for restoring endoplasmic reticulum (ER) homeostasis in response to ER stress. Perturbation of the UPR and failure to restore ER homeostasis inevitably leads to diseases. It has now become evident that perturbation of the UPR is the cause of many important human diseases such as neurodegenerative diseases, cystic fibrosis, diabetes and cancer. It has recently emerged that virus infections can trigger the UPR but the relationship between virus infections and host UPR is intriguing. On one hand, UPR is harmful to the virus and virus has developed means to subvert the UPR. On the other hand, virus exploits the host UPR to assist in its own infection, gene expression, establishment of persistence, reactivation from latency and to evade the immune response. When this delicate balance of virus-host UPR interaction is broken down, it may cause diseases. This is particularly challenging for viruses that establish a chronic infection to maintain this balance. Each virus interacts with the host UPR in a different way to suit their life style and how the virus interacts with the host UPR can define the characteristic of a particular virus infection. Understanding how a particular virus interacts with the host UPR may pave the way to the design of a new class of anti-viral that targets this particular pathway to skew the response towards anti-virus. This knowledge can also be translated into the clinics to help re-design oncolytic virotherapy and gene therapy. In this research topic we aimed to compile a collection of focused review articles, original research articles, commentary, opinion, hypothesis and methods to highlight the current advances in this burgeoning area of research, in an attempt to provide an in-depth understanding of how viruses interact with the host UPR, which may be beneficial to the future combat of viral and human diseases.

Virus diseases. --- Viruses. --- ERAD --- virus-host interaction --- innate immunity --- Gene Therapy --- Pathogenesis --- Endoplasmic Reticulum Stress --- Unfolded Protein Response --- Autophagy

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The endoplasmic reticulum (ER) is an organelle crucial to many cellular functions and processes, including the mounting of T-cell immune responses. Indeed, the ER has a well-established central role in anti-tumor immunity. Perhaps best characterized is the role of the ER in the processing of antigen peptides and the subsequent peptide assembly into MHC class I and II molecules. Such MHC/tumor-derived peptide complexes are pivotal for the correct recognition of altered self or viral peptides and the subsequent clonal expansion of tumor-reactive T-cells. In line with the role of the ER in immunity, tumor-associated mutations in ER proteins, as well as ER protein content and localization can have both deleterious and advantageous effects on anti-tumor immune responses. For instance, loss of function of ER-aminopeptidases, that trim peptides to size for MHC, alter the MHC class I - peptide repertoire thereby critically and negatively affecting T-cell recognition. On the other hand, altered localization of ER proteins can have immune-promoting effects. Specifically, translocation of certain ER proteins to the cell surface has been shown to promote anti-tumor T-cell immunity by directing uptake of apoptotic tumor cells to professional antigen presenting cells, thereby facilitating anti-tumor T-cell immunity. These selected examples highlight a diverse and multi-faceted role of the ER in anti-tumor immunity. Molecular biological insights from the past decade have uncovered that ER components may affect tumor immunity and have invoked a variety of follow-up questions. For instance, how and why are ER proteins over-expressed in tumors? How do nucleotide and somatic mutations in ER chaperones/processing machinery affect the MHC/peptide complex and tumor cell immunogenicity? How do ER-proteins translocate to the cell surface? What if any is the potential role of extracellular ER protein in tumor immunotherapy/vaccines, and can they be delivered to the tumor cell surface by photodynamic therapy, anthracyclines or by other means? In this special research topics issue, we welcome basic and clinical research reports covering all aspects of ER proteins in cancer recognition by the immune system, therapy and drug development. We also welcome reports describing new insights into ER stress, signalling and homeostasis in immunogenic cell death in cancer, the effect of parasitic ER proteins on tumour growth, ER protein regulation of angiogenesis. Submission of original research articles, perspective, reviews and topical comments is encouraged. We aim to provide a comprehensive series of articles that will aid our understanding in a new and exiting avenue of tumour immunology and therapeutic development, exploiting a collection of proteins within the ER that are not obvious candidates for immunity to tumors.

Endoplasmic reticulum. --- Tumors --- Immunology. --- Oncology. --- Endoplasmic Reticulum Stress. --- Autoimmunity --- Angiogenesis --- T-cell receptors --- genome damage --- phage display --- Aminopeptidases --- Grp170 --- Oxidoreductases --- Vaccines --- chaperones --- Immunological aspects.

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The endoplasmic reticulum (ER) is an organelle crucial to many cellular functions and processes, including the mounting of T-cell immune responses. Indeed, the ER has a well-established central role in anti-tumor immunity. Perhaps best characterized is the role of the ER in the processing of antigen peptides and the subsequent peptide assembly into MHC class I and II molecules. Such MHC/tumor-derived peptide complexes are pivotal for the correct recognition of altered self or viral peptides and the subsequent clonal expansion of tumor-reactive T-cells. In line with the role of the ER in immunity, tumor-associated mutations in ER proteins, as well as ER protein content and localization can have both deleterious and advantageous effects on anti-tumor immune responses. For instance, loss of function of ER-aminopeptidases, that trim peptides to size for MHC, alter the MHC class I - peptide repertoire thereby critically and negatively affecting T-cell recognition. On the other hand, altered localization of ER proteins can have immune-promoting effects. Specifically, translocation of certain ER proteins to the cell surface has been shown to promote anti-tumor T-cell immunity by directing uptake of apoptotic tumor cells to professional antigen presenting cells, thereby facilitating anti-tumor T-cell immunity. These selected examples highlight a diverse and multi-faceted role of the ER in anti-tumor immunity. Molecular biological insights from the past decade have uncovered that ER components may affect tumor immunity and have invoked a variety of follow-up questions. For instance, how and why are ER proteins over-expressed in tumors? How do nucleotide and somatic mutations in ER chaperones/processing machinery affect the MHC/peptide complex and tumor cell immunogenicity? How do ER-proteins translocate to the cell surface? What if any is the potential role of extracellular ER protein in tumor immunotherapy/vaccines, and can they be delivered to the tumor cell surface by photodynamic therapy, anthracyclines or by other means? In this special research topics issue, we welcome basic and clinical research reports covering all aspects of ER proteins in cancer recognition by the immune system, therapy and drug development. We also welcome reports describing new insights into ER stress, signalling and homeostasis in immunogenic cell death in cancer, the effect of parasitic ER proteins on tumour growth, ER protein regulation of angiogenesis. Submission of original research articles, perspective, reviews and topical comments is encouraged. We aim to provide a comprehensive series of articles that will aid our understanding in a new and exiting avenue of tumour immunology and therapeutic development, exploiting a collection of proteins within the ER that are not obvious candidates for immunity to tumors.

Endoplasmic reticulum. --- Tumors --- Immunology. --- Oncology. --- Endoplasmic Reticulum Stress. --- Immunological aspects. --- Autoimmunity --- Angiogenesis --- T-cell receptors --- genome damage --- phage display --- Aminopeptidases --- Grp170 --- Oxidoreductases --- Vaccines --- chaperones

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The Special Issue “Marine Anti-Inflammatory and Antioxidants Agents 2021” collected the latest research, both in vitro and in vivo, on natural compounds from a variety of deep-sea organisms with anti-inflammatory and/or antioxidant properties as potential candidates for new drug discovery, and more generally for the field of marine biotechnology. The research presented here discusses the potential benefits of certain peptides and proteins derived from oysters, blue mussels, and cyanobacteria, as well as the carotenoid pigment astaxanthin, which is found in a variety of marine organisms. This Special Issue has carved out an important space for crude extracts from marine products, such as microalgae and green algae, highlighting their potential benefits to human health. Finally, the Special Issue includes a review of the benefits of some natural compounds derived from the algal biome against inflammatory bowel diseases, as well as a research article identifying the presence of the OvoA gene in arthropods for the first time. Through an excursus of high-quality research, this Special Issue provides the entire scientific community with new tools and insights to catch a molecular treasure for human health from the sea.

Medicine --- Pharmacology --- algal biome --- polysaccharides --- bioactive entities --- engineered cues --- therapeutic attributes --- inflammatory bowel disease --- microalgae --- Tisochrysis lutea --- fucoxanthin --- inflammation --- RAW 264.7 --- microRNA --- astaxanthin --- dendritic cells --- sepsis --- immune dysfunction --- lipopolysaccharide --- oxidative stress --- Ulva lactuca --- polysaccharide --- D-galactose --- kidney --- oyster peptides --- spermatogenesis --- apoptosis --- hormone --- testis --- C-phycoerythrin --- Phormidium persicinum --- acute kidney injury --- mercury --- endoplasmic reticulum stress --- bioactive peptide --- cytoprotective --- endothelial dysfunction --- blue mussel --- acute liver injury --- ferroptosis --- oyster --- peptide --- pyroptosis --- zooplankton --- natural products --- antioxidant --- transcriptome mining --- n/a