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Статті в журналах з теми "Alarmine HMGB1"
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De Martinis, Massimo, Lia Ginaldi, Maria Maddalena Sirufo, Giovanni Pioggia, Gioacchino Calapai, Sebastiano Gangemi, and Carmen Mannucci. "Alarmins in Osteoporosis, RAGE, IL-1, and IL-33 Pathways: A Literature Review." Medicina 56, no. 3 (March 19, 2020): 138. http://dx.doi.org/10.3390/medicina56030138.
Повний текст джерелаАнотація:
Alarmins are endogenous mediators released by cells following insults or cell death to alert the host’s innate immune system of a situation of danger or harm. Many of these, such as high-mobility group box-1 and 2 (HMGB1, HMGB2) and S100 (calgranulin proteins), act through RAGE (receptor for advanced glycation end products), whereas the IL-1 and IL-33 cytokines bind the IL-1 receptors type I and II, and the cellular receptor ST2, respectively. The alarmin family and their signal pathways share many similarities of cellular and tissue localization, functions, and involvement in various physiological processes and inflammatory diseases including osteoporosis. The aim of the review was to evaluate the role of alarmins in osteoporosis. A bibliographic search of the published scientific literature regarding the role of alarmins in osteoporosis was organized independently by two researchers in the following scientific databases: Pubmed, Scopus, and Web of Science. The keywords used were combined as follows: “alarmins and osteoporosis”, “RAGE and osteoporosis”, “HMGB1 and osteoporosis”, “IL-1 and osteoporosis”, “IL 33 and osteopororsis”, “S100s protein and osteoporosis”. The information was summarized and organized in the present review. We highlight the emerging roles of alarmins in various bone remodeling processes involved in the onset and development of osteoporosis, as well as their potential role as biomarkers of osteoporosis severity and progression. Findings of the research suggest a potential use of alarmins as pharmacological targets in future therapeutic strategies aimed at preventing bone loss and fragility fractures induced by aging and inflammatory diseases.
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Lu, Huijiao, Mengyi Zhu, Lin Qu, Hongwei Shao, Rongxin Zhang, and Yan Li. "Oncogenic Role of HMGB1 as an Alarming in Robust Prediction of Immunotherapy Response in Colorectal Cancer." Cancers 14, no. 19 (October 5, 2022): 4875. http://dx.doi.org/10.3390/cancers14194875.
Повний текст джерелаАнотація:
Objective: To assess the correlation between HMGB1 expression and the patient prognosis in a multicancer context. Methods: The potential oncogenic role of HMGB1 was explored in forty tumors through the TCGA, GEO, and Oncomine datasets. We analyzed the clinical prognostic value and antitumor immunotherapy of HMGB1 in a multicancer context using GEO (GSE111636). Results: High expression of HMGB1 is present in multicancer cases, and its low expression is closely associated with the prognostic survival of patients, in terms of both overall and disease-free survival in ACC and LUAD. Further investigation revealed that the high expression of gastric and lung cancer is closely associated with low risk and better prognosis of patients based on COX and Kaplan–Meier analysis of OS, FP and PPS. HMGB1 expression was found to be significantly correlated with cancer-associated fibroblast and CD8+ T cell infiltration in the TME. The analysis of GO functional annotation/KEGG pathways indicates that HMGB1 may regulate tumor immunity-related pathways, such as the tumor immunotherapy response in colorectal cancer. The function of four genes as hubs are confirmed by in vitro HMGB1 knockdown which led to inhibition of cell proliferation and metastasis in SW620 and SW480 cells. Conclusion: HMGB1 is a potential novel biomarker for improving clinical prognosis and antitumor immunotherapy efficacy. CDK1, HMGB2, SSRP1, and H2AFV may serve as key nodes for HMGB1 in colorectal cancer.
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Palumbo, Antonino, Fabiola Atzeni, Giuseppe Murdaca, and Sebastiano Gangemi. "The Role of Alarmins in Osteoarthritis Pathogenesis: HMGB1, S100B and IL-33." International Journal of Molecular Sciences 24, no. 15 (July 29, 2023): 12143. http://dx.doi.org/10.3390/ijms241512143.
Повний текст джерелаАнотація:
Osteoarthritis (OA) is a multifactorial disease in which genetics, aging, obesity, and trauma are well-known risk factors. It is the most prevalent joint disease and the largest disability problem worldwide. Recent findings have described the role of damage-associated molecular patterns (DAMPs) in the course of the disease. In particular, alarmins such as HMGB1, IL-33, and S100B, appear implicated in enhancing articular inflammation and favouring a catabolic switch in OA chondrocytes. The aims of this review are to clarify the molecular signalling of these three molecules in OA pathogenesis, to identify their possible use as staging biomarkers, and, most importantly, to find out whether they could be possible therapeutic targets. Osteoarthritic cartilage expresses increased levels of all three alarmins. HMGB1, in particular, is the most studied alarmin with increased levels in cartilage, synovium, and synovial fluid of OA patients. High levels of HMGB1 in synovial fluid of OA joints are positively correlated with radiological and clinical severity. Counteracting HMGB1 strategies have revealed improving results in articular cells from OA patients and in OA animal models. Therefore, drugs against this alarmin, such as anti-HMGB1 antibodies, could be new treatment possibilities that can modify the disease course since available medications only alleviate symptoms.
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Casciaro, Marco, Eleonora Di Salvo, and Sebastiano Gangemi. "HMGB-1 in Psoriasis." Biomolecules 12, no. 1 (December 31, 2021): 60. http://dx.doi.org/10.3390/biom12010060.
Повний текст джерелаАнотація:
Psoriasis is a multifactorial pathology linked to systemic inflammation. Enhanced keratinocytes proliferation and a minor maturation state of the cells are typical features. Perivascular T cells, dendritic cells, macrophages, and neutrophilic granulocytes are part of the scenario completed by apoptosis dysregulation. Several proinflammatory mediators, alarmins and growth factors are increased too, both in the skin and the patients’ blood. HMGB1 is important as an alarmin in several inflammatory conditions. Released after cellular damage, HMGB1 acts as a danger signal. Several studies have considered its role in psoriasis pathogenesis. We evaluated its level in psoriasis and the potential of the alarmin blockade through standard therapies, biological treatments and using monoclonal antibodies. PV patients were shown to have significantly increased levels of HMGB1 both in lesional skin and in serum, which were linked, in some cases, to other pro-inflammatory markers and alarmins. In most cases these parameters were correlated with PASI score. Data demonstrated that blocking HMGB1 is effective in ameliorating psoriasis. Focusing on this approach could be valuable in terms of a therapeutic option for counteracting immune-related diseases in a way unthinkable until few years ago.
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Yang, De, Yuri V. Postnikov, Yana Li, Poonam Tewary, Gonzalo de la Rosa, Feng Wei, Dennis Klinman, et al. "High-mobility group nucleosome-binding protein 1 acts as an alarmin and is critical for lipopolysaccharide-induced immune responses." Journal of Experimental Medicine 209, no. 1 (December 19, 2011): 157–71. http://dx.doi.org/10.1084/jem.20101354.
Повний текст джерелаАнотація:
Alarmins are endogenous mediators capable of promoting the recruitment and activation of antigen-presenting cells (APCs), including dendritic cells (DCs), that can potentially alert host defense against danger signals. However, the relevance of alarmins to the induction of adaptive immune responses remains to be demonstrated. In this study, we report the identification of HMGN1 (high-mobility group nucleosome-binding protein 1) as a novel alarmin and demonstrate that it contributes to the induction of antigen-specific immune responses. HMGN1 induced DC maturation via TLR4 (Toll-like receptor 4), recruitment of APCs at sites of injection, and activation of NF-κB and multiple mitogen-activated protein kinases in DCs. HMGN1 promoted antigen-specific immune response upon co-administration with antigens, and Hmgn1−/− mice developed greatly reduced antigen-specific antibody and T cell responses when immunized with antigens in the presence of lipopolysaccharide (LPS). The impaired ability of Hmgn1−/− mice to mount antigen-specific immune responses was accompanied by both deficient DC recruitment at sites of immunization and reduced production of inflammatory cytokines. Bone marrow chimera experiments revealed that HMGN1 derived from nonleukocytes was critical for the induction of antigen-specific antibody and T cell responses. Thus, extracellular HMGN1 acts as a novel alarmin critical for LPS-induced development of innate and adaptive immune responses.
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Jiang, Lili, Yijia Shao, Yao Tian, Changsheng Ouyang, and Xiaohua Wang. "Nuclear Alarmin Cytokines in Inflammation." Journal of Immunology Research 2020 (December 4, 2020): 1–8. http://dx.doi.org/10.1155/2020/7206451.
Повний текст джерелаАнотація:
Pathogen-associated molecular patterns (PAMPs) are some nonspecific and highly conserved molecular structures of exogenous specific microbial pathogens, whose products can be recognized by pattern recognition receptor (PRR) on innate immune cells and induce an inflammatory response. Under physiological stress, activated or damaged cells might release some endogenous proteins that can also bind to PRR and cause a harmful aseptic inflammatory response. These endogenous proteins were named damage-associated molecular patterns (DAMPs) or alarmins. Indeed, alarmins can also play a beneficial role in the tissue repair in certain environments. Besides, some alarmin cytokines have been reported to have both nuclear and extracellular effects. This group of proteins includes high-mobility group box-1 protein (HMGB1), interleukin (IL)-33, IL-1α, IL-1F7b, and IL-16. In this article, we review the involvement of nuclear alarmins such as HMGB1, IL-33, and IL-1α under physiological state or stress state and suggest a novel activity of these molecules as central initiators in the development of sterile inflammation.
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Briquet, Sylvie, Nadou Lawson-Hogban, Bertrand Boisson, Miguel P. Soares, Roger Péronet, Leanna Smith, Robert Ménard, Michel Huerre, Salah Mécheri, and Catherine Vaquero. "Disruption of Parasitehmgb2Gene Attenuates Plasmodium berghei ANKA Pathogenicity." Infection and Immunity 83, no. 7 (April 27, 2015): 2771–84. http://dx.doi.org/10.1128/iai.03129-14.
Повний текст джерелаАнотація:
Eukaryotic high-mobility-group-box (HMGB) proteins are nuclear factors involved in chromatin remodeling and transcription regulation. When released into the extracellular milieu, HMGB1 acts as a proinflammatory cytokine that plays a central role in the pathogenesis of several immune-mediated inflammatory diseases. We found that thePlasmodiumgenome encodes two genuine HMGB factors,PlasmodiumHMGB1 and HMGB2, that encompass, like their human counterparts, a proinflammatory domain. Given that these proteins are released from parasitized red blood cells, we then hypothesized thatPlasmodiumHMGB might contribute to the pathogenesis of experimental cerebral malaria (ECM), a lethal neuroinflammatory syndrome that develops in C57BL/6 (susceptible) mice infected withPlasmodium bergheiANKA and that in many aspects resembles human cerebral malaria elicited byP. falciparuminfection. The pathogenesis of experimental cerebral malaria was suppressed in C57BL/6 mice infected withP. bergheiANKA lacking thehmgb2gene (Δhmgb2ANKA), an effect associated with a reduction of histological brain lesions and with lower expression levels of several proinflammatory genes. The incidence of ECM inpbhmgb2-deficient mice was restored by the administration of recombinantPbHMGB2. Protection from experimental cerebral malaria in Δhmgb2ANKA-infected mice was associated with reduced sequestration in the brain of CD4+and CD8+T cells, including CD8+granzyme B+and CD8+IFN-γ+cells, and, to some extent, neutrophils. This was consistent with a reduced parasite sequestration in the brain, lungs, and spleen, though to a lesser extent than in wild-typeP. bergheiANKA-infected mice. In summary,PlasmodiumHMGB2 acts as an alarmin that contributes to the pathogenesis of cerebral malaria.
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Yang, De, Yuri Postnikov, Yana Li, Poonam Tewary, Gonzalo de la Rosa, Dennis Kliman, Takashi Furusawa, Michael Bustin, Feng Wei, and Joost Oppenheim. "High mobility group nucleosome-binding protein 1 acts as an alarmin critical for the induction of immune response (113.7)." Journal of Immunology 186, no. 1_Supplement (April 1, 2011): 113.7. http://dx.doi.org/10.4049/jimmunol.186.supp.113.7.
Повний текст джерелаАнотація:
Abstract Alarmins, defined as endogenous mediator(s) capable of promoting the recruitment and activation of antigen-presenting cells (APCs) including dendritic cells (DCs), can potentially promote immunity, however, their essential contribution to the induction immune responses remain to be demonstrated. Here we report the identification of HMGN1 as a novel alarmin that is critical to the induction of antigen-specific immune response. HMGN1 induced DC maturation and recruitment of APCs and activated NF-κB and multiple MAPKs, in a MyD88-dependent manner. HMGN1 promoted antigen-specific immune response upon co-administration with an antigen. Furthermore, knockout of HMGN1 in mice greatly reduced antigen-specific antibody and T cell responses upon intraperitoneal immunization with an antigen using LPS as an adjuvant. The impaired ability of HMGN1 KO mice to mount antigen-specific immune responses was accompanied by both deficient DC recruitment at sites of immunization and reduced production of inflammatory cytokines. Bone marrow chimera experiments revealed that HMGN1 derived from non-leukocytes played a more critical role in the induction of antigen-specific antibody and T cell responses. Thus, HMGN1 acts as a novel alarmin critical for the induction of adaptive immune response.
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Bidwell, Joseph P., Jieping Yang, and Alexander G. Robling. "Is HMGB1 an osteocyte alarmin?" Journal of Cellular Biochemistry 103, no. 6 (2008): 1671–80. http://dx.doi.org/10.1002/jcb.21572.
Повний текст джерела
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Mezentsev, A. V., E. V. Denisova, V. V. Sobolev, and I. M. Korsunskaya. "The role of alarmins in the pathogenesis of psoriasis." Meditsinskiy sovet = Medical Council, no. 14 (September 28, 2023): 62–70. http://dx.doi.org/10.21518/ms2023-276.
Повний текст джерелаАнотація:
Alarmins are a group of immune activating proteins/peptides that initiate an inflammatory process by interacting with immune cells. The alarmins are biosynthesized as a result of cell injury, often due to proteolysis of native proteins. Most often, the alarmins are released into the extracellular matrix as a result of infection, burn or trauma. Several studies have been conducted recently to determine the role of alarmins in the pathogenesis of autoimmune diseases. This work was aimed to assess the clinical potential of alarmins and characterize their role in the pathogenesis of psoriasis. The proposed review analysed 6 groups of alarmins with increased expression in the skin of patients with psoriasis: defensins, CAMP/LL-37, amphoterin/HMGB1, interleukin-1 (IL-1)-like cytokine family members (IL1 and -33) with alarmin properties, heat shock proteins, and proteins of the S100 family. The presented work also discusses the therapeutic potential of alarmins: the possibility to use them as the drug therapy target, as well as to establish diagnosis and monitor the progress of psoriasis. The further experimental studies are supposed to pay considerable attention to alarmin receptors, as well as members involved in the signalling pathways they initiated. These work findings help to obtain biologically active compounds that will be able to specifically and effectively inhibit the physiological effects of alarmins, as well as control the inflammatory process they induced. It seems certain that the use of alarmin antagonists in clinical practice will prove useful in the treatment of both psoriasis and other chronic autoimmune diseases, especially in cases where the most commonly used therapies are not effective enough.
Дисертації з теми "Alarmine HMGB1"
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Lorvellec, Marie. "Dialogue entre le complément C1 et l'alarmine HMGB1 dans l'inflammation." Electronic Thesis or Diss., Université Grenoble Alpes, 2024. http://www.theses.fr/2024GRALV033.
Повний текст джерелаАнотація:
La protéase C1s est un élément central dans l’initiation de la voie classique du système du complément. Elle était auparavant considérée comme ciblant exclusivement les protéines C2 et C4 dans cette cascade protéolytique. Des découvertes récentes ont cependant mis en lumière la présence de C1s libre constitutivement active dans certaines pathologies, suggérant un rôle plus large de cette protéase au-delà de l'activation du complément. Parmi les cibles non-canoniques identifiées de C1s figure la protéine HMGB1, initialement décrite comme une protéine nucléaire impliquéedans la condensation de la chromatine et l'expression des gènes. Des études récentes ont démontré que HMGB1 peut également être localisée dans différents compartiments cellulaires et qu'elle joue un rôle crucial dans l'inflammation lorsqu'elle est libérée dans le milieu extracellulaire. Ce projet de thèse avait pour objectif principal d'élucider le rôle du clivage de HMGB1 par C1s dans la modulation de la réponse inflammatoire. Nos travaux ont démontré que les fragments de digestion de HMGB1 possèdent des effets distincts de la protéine entière sur l'activation du complément et laréponse cytokinique des macrophages. Nous avons notamment confirmé que la protéine entière active la voie classique du complément lorsqu’elle est fixée à une surface et qu’elle favorise la polarisation M1 des macrophages en réponse aux LPS. En revanche, le fragment f2 est capable d'activer la voie classique du complément même lorsqu’il est en solution, tandis que le fragment f3 inhibe la sécrétion de cytokines pro-inflammatoires dans les études cellulaires. De plus, nous avons exploré l'impact de l'état d'oxydo-réduction des cystéines sur les effets de HMGB1 et de ses fragmentsen utilisant des mutants mimétiques. La digestion de HMGB1 est restreinte lorsque la protéine est sous forme disulfure, suggérant un rôle important du pont disulfure dans l’accès aux sites de digestion par C1s. Les formes redox de la protéine entière ne semblent pas affecter sa capacité à activer le complément, tandis que le fragment f2 oxydé pourrait perdre sa capacité d'activation en solution. Ces résultats révèlent que le clivage de HMGB1 par C1s agit comme un chronomètre de l’inflammation, orchestrant la réponse inflammatoire via la transition d’une phase d’amplification pro-inflammatoireà une phase de résolution. Ces découvertes ouvrent de nouvelles perspectives pour la compréhension des mécanismes complexes de l'inflammation et le développement de thérapies pour le traitement de pathologies inflammatoiresC1s protease is a central component in the initiation of the classical pathway of the complement system. It was originally believed to exclusively target proteins C2 and C4 in this proteolytic cascade. However, recent discoveries have highlighted the presence of constitutively active free C1s in certain pathologies, suggesting a broader role for this protease beyond complement activation. Among the non-canonical targets identified for C1s is the HMGB1 protein, initially described as a nuclear protein involved in chromatin condensation and gene expression.Recent studies have shown that HMGB1 can also be localized in different cellular compartments and plays a crucial role in inflammation when released into the extracellular environment. The main objective of this thesis project was to elucidate the role of C1s cleavage of HMGB1 in modulating the inflammatory response. Our work has shown that HMGB1 digestion fragments have distinct effects from the whole protein on complement activation and macrophage cytokine responses.In particular, we confirmed that the whole protein activates the classical complement pathway when bound to a surface and promotes M1 macrophage polarization in response to LPS. In contrast, fragment f2 is capable of activating the classical complement pathway, even when in solution, while fragment f3 inhibits the secretion of pro-inflammatory cytokines in cell studies. In addition, we explored the impact of cysteine redox state on the effects of HMGB1 and its fragments using mimetic mutants. HMGB1 digestion is restricted when the protein is in disulfide form, suggesting an important role of the disulfide bridge in access to the C1s digestion site. The redox forms of the whole protein do notappear to affect its ability to activate complement, while oxidized fragment f2 may lose its ability to activate it in solution. These results reveal that C1s cleavage of HMGB1 acts as an inflammation timer, orchestrating the inflammatory response through the transition from a pro-inflammatory amplification phase to a resolution phase. These findings open new perspectives for understanding the complex mechanisms of inflammation and the development of therapies for the treatment of inflammatory diseases
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Sigaut, Stéphanie. "Activation microgliale : mécanismes et conséquences à long terme." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCC198/document.
Повний текст джерелаАнотація:
La neuro-inflammation induite par l'inflammation systémique ou générée en réponse à une lésion cérébrale aiguë a des conséquences cliniques néfastes : elle est mise en cause dans l'aggravation des lésions cérébrales aiguës chez l'homme, aussi bien chez l'adulte que chez l'enfant. La microglie est l'effecteur cérébral principal de cette réponse inflammatoire, et peut présenter selon les situations un profil neurotoxique ou, au contraire, anti-inflammatoire et régulateur. La compréhension des mécanismes d'activation microgliale et de leurs conséquences est capitale pour une meilleure prise en charge des malades. La première partie de ce travail de thèse s'intéresse aux conséquences de l'inflammation néonatale associée à la prématurité sur la réponse microgliale à l'âge adulte, face à de nouvelles agressions cérébrales que sont l'inflammation systémique et les lésions cérébrales aiguës. Dans un modèle murin d'inflammation néonatale, nous avons mis en évidence d'importantes modifications du transcriptome microglial une fois ces souris adultes. De plus, un stimulus inflammatoire à l'âge adulte modifie le profil d'activation microgliale, le pic des marqueurs pro-inflammatoires et immuno-régulateurs survenant plus précocement et intensément, démontrant l'existence d'une mémoire du système immunitaire inné cérébral. Ces modifications dans le profil d'activation microgliale s'accompagnent dans un modèle de lésion cérébrale excitotoxique d'une majoration de la taille des lésions de la substance blanche. Un traitement par mélatonine des souriceaux prévient cette aggravation. La deuxième partie de ce travail a consisté à caractériser in vitro le profil d'activation microgliale en réponse à une stimulation par HMGB1, une alarmine relarguée lors de la mort cellulaire et donc présente en cas de lésion cérébrale aiguë mais aussi de lésions extra-crâniennes associées. Nous avons montré que le profil d'activation microgliale dépend du type d'HMGB1 utilisé. Les microglies exposées à la forme recombinante de chez Sigma présentent un profil transcriptomique proinflammatoire mais une baisse des taux de cytokines sécrétées dans le milieu. Ces résultats mettent en évidence l'importance de l'inflammation et de l'activation microgliale dans le pronostic des lésions cérébrales et offrent la possibilité de mettre en place des stratégies neuroprotectrices innovantesNeuroinflammation induced by systemic inflammation or generated in response to acute brain injury has adverse clinical consequences: it is implicated in exacerbation of acute brain injury in humans, for adults as well as for children. Microglia is the main effector of this cerebral inflammatory response, and may present, depending on the situation, a neurotoxic or - on the opposite - anti-inflammatory and regulating profile. To decipher the mechanisms of microglial activation and their consequences is essential for better management of patients.The first part of this thesis focuses on the consequences of neonatal inflammation associated with prematurity on the microglial response in adulthood, in case of new cerebral aggressions such as systemic inflammation or acute brain injury. Relying on a mouse model of inflammation of the preterm infant, we have demonstrated drastic modifications of the microglial transcriptome once these mice are adults. Moreover, when an inflammatory stimulus occurs in adulthood, the microglial activation profile is altered, the peak of pro-inflammatory and immuno-regulatory markers occurring earlier, demonstrating the existence of a memory of the cerebral innate immune system. These changes in the microglial activation profile are accompanied in a model of excitotoxic brain injury by an increase of the white matter lesion size. Melatonin treatment of mice prevents the happening of this worse outcome. In the second part of this thesis, we characterized the microglial activation profile in vitro, in response to stimulation by HMGB1, a damage associated molecular pattern released during cell death and therefore present in acute brain injuries but also in associated extra-cranial injuries. We have shown that the microglial activation profile depends of the kind of HMGB1 used. Microglia exposed to Sigma recombinant form have a proinflammatory transcriptomic profile but a lower release of cytokines in the culture medium. These results highlight the importance of inflammation and microglial activation in the prognosis of brain injuries and offer the opportunity to implement innovative neuroprotective strategies
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Bremer, Lisa. "Hyaluronan (HA) fragments as initiators or enhancers of inflammation in arthritis." Thesis, KTH, Skolan för bioteknologi (BIO), 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-215225.
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Malamis, Dimitrios. "Systemic levels of inflammatory mediators in periodontitis." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1436961245.
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"Molecular Mechanisms Regulating the Activation of Eosinophils Induced by S. aureus–associated NOD2/TLR2 Ligands, Alarmin HMGB1 and Antimicrobial Peptide LL-37 in Allergic Inflammation." 2016. http://repository.lib.cuhk.edu.hk/en/item/cuhk-1292458.
Повний текст джерелаТези доповідей конференцій з теми "Alarmine HMGB1"
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Fölsch, K., A. Volmari, CF Manthey, AW Lohse, S. Huber, and P. Hübener. "Intestinale Entzündung und Karzinogenese werden durch das Alarmin HMGB1 reguliert." In Viszeralmedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1695395.
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Davalos, Albert R., Misako Kawahara, Gautam K. Malhotra, Jiahao Huang, Urvi Ved, Francis Rodier, Christian Beausejour, Jean Philippe Coppe, and Judith Campisi. "Abstract A3: p53-dependent release of alarmin HMGB1 is a central mediator of senescent phenotypes." In Abstracts: Second AACR International Conference on Frontiers in Basic Cancer Research--Sep 14-18, 2011; San Francisco, CA. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.fbcr11-a3.
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Davalos, Albert R., Misako Kawahara, Gautam Malhotra, Christian Beausejour, Francis Rodier, and Judith Campisi. "Abstract LB-483: p53-dependent release of Alarmin HMGB1 is a central mediator of senescent phenotypes." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-lb-483.
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Rozycki, Henry J., Adam Brock, Melissa Yopp, Christopher Corday, Shauna Webb-Parker, and Tsuyoshi Tanabe. "Increased CXCL2 Production From Mouse Type II Alveolar Epithelial Cells In Response To The Alarmin HMGB1." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4269.
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