Добірка наукової літератури з теми "Arthritogenic"
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Статті в журналах з теми "Arthritogenic"
Šimelyte, Egle, Marja Rimpiläinen, Leena Lehtonen, Xiang Zhang, and Paavo Toivanen. "Bacterial Cell Wall-Induced Arthritis: Chemical Composition and Tissue Distribution of Four Lactobacillus Strains." Infection and Immunity 68, no. 6 (June 1, 2000): 3535–40. http://dx.doi.org/10.1128/iai.68.6.3535-3540.2000.
Повний текст джерелаMejía, Carla-Ruth, and Rogelio López-Vélez. "Tropical Arthritogenic Alphaviruses." Reumatología Clínica (English Edition) 14, no. 2 (March 2018): 97–105. http://dx.doi.org/10.1016/j.reumae.2017.01.005.
Повний текст джерелаRao, Shambhavi, and Adam Taylor. "Arthritogenic Alphavirus Capsid Protein." Life 11, no. 3 (March 11, 2021): 230. http://dx.doi.org/10.3390/life11030230.
Повний текст джерелаArcher, J. R., and M. A. Whelan. "HLA-B27 and effector T cells: arthritogenic peptide or arthritogenic antigen?" Lancet 342, no. 8882 (November 1993): 1307. http://dx.doi.org/10.1016/0140-6736(93)92402-f.
Повний текст джерелаMostafavi, Helen, Eranga Abeyratne, Ali Zaid, and Adam Taylor. "Arthritogenic Alphavirus-Induced Immunopathology and Targeting Host Inflammation as A Therapeutic Strategy for Alphaviral Disease." Viruses 11, no. 3 (March 22, 2019): 290. http://dx.doi.org/10.3390/v11030290.
Повний текст джерелаSuhrbier, Andreas, Marie-Christine Jaffar-Bandjee, and Philippe Gasque. "Arthritogenic alphaviruses—an overview." Nature Reviews Rheumatology 8, no. 7 (May 8, 2012): 420–29. http://dx.doi.org/10.1038/nrrheum.2012.64.
Повний текст джерелаAbdelnabi, Rana, and Leen Delang. "Antiviral Strategies against Arthritogenic Alphaviruses." Microorganisms 8, no. 9 (September 7, 2020): 1365. http://dx.doi.org/10.3390/microorganisms8091365.
Повний текст джерелаRodríguez-Morales, Alfonso J., Jorge A. Sánchez-Duque, and Juan-Manuel Anaya. "Response to: Tropical Arthritogenic Alphaviruses." Reumatología Clínica (English Edition) 14, no. 4 (July 2018): 245–46. http://dx.doi.org/10.1016/j.reumae.2017.07.004.
Повний текст джерелаInglis, TimothyJ. "DIETARY LIPOPOLYSACCHARIDES AS ARTHRITOGENIC ANTIGEN?" Lancet 329, no. 8527 (January 1987): 274. http://dx.doi.org/10.1016/s0140-6736(87)90092-4.
Повний текст джерелаPettipher, E. R., G. A. Higgs, and B. Henderson. "Arthritogenic activity of interleukin 1." Agents and Actions 19, no. 5-6 (December 1986): 337–38. http://dx.doi.org/10.1007/bf01971244.
Повний текст джерелаДисертації з теми "Arthritogenic"
Lundberg, Karin. "Arthritogenic and immunogenic properties of modified autoantigens /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-303-5/.
Повний текст джерелаSchönwetter-Steer, Margarete [Verfasser], and Elisabeth [Akademischer Betreuer] Weiss. "Analyse autoreaktiver T-Zellen zur Identifizierung arthritogener Peptide bei der HLA-B27-assoziierten reaktiven Arthritis / Margarete Schönwetter-Steer. Betreuer: Elisabeth Weiss." München : Universitätsbibliothek der Ludwig-Maximilians-Universität, 2014. http://d-nb.info/1112038973/34.
Повний текст джерелаSilva, Daniela Filipa Amaral. "Functional characterization of arthritogenic T cells." Master's thesis, 2017. http://hdl.handle.net/10316/83149.
Повний текст джерелаA artrite reumatóide (AR) é a doença autoimune reumática crónica mais comum, afectando 0,5-1% da população mundial. A incidência desta doença autoimune é três vezes superior nas mulheres do que nos homens, com idades entre 40-70 anos. A etiologia da doença permanece desconhecida, embora a combinação de factores hormonais, genéticos, sexuais e ambientais sejam importantes contribuintes para o desenvolvimento de AR. Várias evidências apoiam o envolvimento directo das células T na patogénese da AR, nomeadamente i) a correlação da susceptibilidade e severidade da AR com os genes associados à activação das células T e a diferenciação de células T anormal, como o antígeno leucocitário humano - antígeno D relacionado (HLA- DR) e a proteína tirosina fosfatase não receptora do tipo 22 (PTPN22); ii) o recrutamento e activação contínua de células T nas articulações de pacientes com AR; iii) a transferência de células T CD4 do sinóvio dos pacientes é suficiente para induzir AR em ratos imunes deficientes. No entanto, a base molecular da desregulação das células T nesta doença permanece indescritível. Os tratamentos biológicos actuais são bem-sucedidos no controlo de AR num subconjunto de pacientes, neutralizando a resposta inflamatória global sem ter como alvo as causas subjacentes que geram inflamação crónica. Embora os tratamentos biológicos tenham aumentado a qualidade de vida de alguns pacientes, nem todos os pacientes respondem à terapia (50%), os tratamentos biológicos têm sérios efeitos colaterais imunossupressores e perdem a eficácia ao longo do tempo. Portanto, existe uma necessidade de desenvolvimento de novas terapias que sejam direccionadas precisamente para os mecanismos subjacentes à desregulação das células T CD4 em vez da activação geral das células T ou dos produtos finais, citoquinas inflamatórias. Apesar do seu papel primordial, muito pouco se sabe sobre a base molecular da desregulação de células T na AR. Este estudo pretende elucidar os circuitos moleculares que controlam a desregulação das células T, bem como, esclarecer como é possível desactivá-las, um conhecimento em última instância necessário para induzir a remissão da AR.No meu trabalho experimental, através da análise de amostras de sangue de pacientes com AR e do uso da técnica de citometria, foi feita uma caracterização das células T existentes. Particularmente, a produção de citoquinas inflamatórias foi medida para caracterizar a resposta das células T na patologia AR. Adicionalmente, alguns circuitos moleculares foram avaliados para fornecer informação sobre a resposta patogénica das células T. O impacto da identificação do circuito molecular das células T envolvidas estende-se muito além da patogénese. Assim, poderá representar um ponto de partida para novas imunoterapias de precisão capazes de reverter a AR sem imunossupressão dos pacientes. A nível clínico, este projeto poderia fornecer biomarcadores para serem usados no diagnóstico pré-sintomático e na monitorização da progressão da doença e da eficiência do tratamento.
Rheumatoid arthritis (RA) is the most common chronic rheumatic autoimmune disease, affecting 0,5-1% of worldwide population. The incidence of this autoimmune disease is three times greater in females than in males, with an age at onset between 40-70 years. The aetiology of the disease remains unknown although the combination of hormonal, genetic, sex and environmental factors are important contributors to the development of RA. Distinct evidence supports the direct involvement of T cells in the pathogenesis of RA, namely i) the correlation of RA susceptibility and severity with genes associated with T cell activation and abnormal T cell differentiation, such as human leukocyte antigen – antigen D related (HLA-DR) and protein tyrosine phosphatase non-receptor type 22 (PTPN22); ii) the continuous recruitment and activation of T cells into the joints of patients with RA; iii) transfer of CD4 T cells from patients synovium is sufficient to induce RA in immune deficient mice. However, the molecular basis of T cell dysregulation in this disease remains elusive.Current biological treatments are successful at managing RA in a subset of patients by quenching the overall inflammatory response without targeting the underlying causes driving chronic inflammation. Even though biological treatments have increased the quality of life of some patients, not all patients respond to therapy (50%), biological treatments have serious immunocompromising side effects and they lose efficiency over time. Therefore, there is an unmet need for therapies that precisely target the mechanisms underpinning CD4 T cell dysregulation rather than overall T cell activation or the end products, inflammatory cytokines. Despite their primordial role, very little is known about the molecular basis of T cell dysregulation in RA. This study aims to elucidate the molecular circuits that control T cell dysregulation and to clarify how to turn them off, a knowledge ultimately necessary to induce RA remission.In my experimental work, by analyzing blood samples from RA patients and by using flow cytometry technique a characterization of existing T cells was made. Particularly, inflammatory cytokines production was measured to characterize the responsiveness of T cells in RA pathology. Additionally, some molecular circuits were evaluated to provide some insights of the pathogenic responses of T cells.The impact of identifying the molecular circuitry of T cells driving RA is well beyond pathogenesis. It could represent the starting ground for new precision immunotherapies capable of reverting RA without immunocompromising the patients. At clinical level, this project could provide biomarkers to be used in pre-symptomatic diagnosis and in monitoring disease progression and treatment efficiency.
Brasted, Melissa. "Effector CD4⁺ T lymphocytes in the prodrome of polyarthritis." Thesis, 2002. http://hdl.handle.net/2440/80103.
Повний текст джерелаThesis (Ph.D.) -- University of Adelaide, Dept. of Molecular Biosciences, 2002
Книги з теми "Arthritogenic"
Siebert, Stefan, Sengupta Raj, and Alexander Tsoukas. The genetics of axial spondyloarthritis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198755296.003.0004.
Повний текст джерелаNoordenbos, Troy, and Dominique Baeten. Immune mechanisms: innate immunity. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0007.
Повний текст джерелаColbert, Robert A., and Paul Bowness. Immune mechanisms: HLA-B27. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198734444.003.0006.
Повний текст джерелаK. Gautam, Rupesh, Lokesh Deb, and Kamal Dua, eds. Natural Products for the Management of Arthritic Disorders. BENTHAM SCIENCE PUBLISHERS, 2022. http://dx.doi.org/10.2174/97898150507761220101.
Повний текст джерелаЧастини книг з теми "Arthritogenic"
Tupanceska, Daniela, Ali Zaid, Nestor E. Rulli, Sandra Thomas, Brett A. Lidbury, Klaus I. Matthaei, Ruben Ramirez, and Suresh Mahalingam. "Ross River Virus: An Arthritogenic Alphavirus of Significant Importance in the Asia Pacific." In Issues in Infectious Diseases, 94–111. Basel: KARGER, 2006. http://dx.doi.org/10.1159/000096693.
Повний текст джерела"Arthritogenic Pain." In Encyclopedia of Pain, 203. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-28753-4_100135.
Повний текст джерелаHerrero, Lara J., Adam Taylor, Suan Sin Foo, Lynden Roberts, Natkunam Ketheesan, and Suresh Mahalingam. "Clinical Manifestations of Arthritogenic Alphaviruses." In Alphaviruses: Current Biology, 125–38. Caister Academic Press, 2016. http://dx.doi.org/10.21775/9781910190159.07.
Повний текст джерелаKONO, DWIGHT H., JIN-HAI CHEN, ASAO NAKAYAMA, and DAVID T. Y. YU. "Mimicry between HLA-B27 and Bacteria: A Spurious Finding or the Link Connecting HLA-B27 and Arthritogenic Bacteria?" In Immune Recognition and Evasion: Molecular Aspects of Host�parasite Interaction, 53–60. Elsevier, 1990. http://dx.doi.org/10.1016/b978-0-12-711710-2.50008-x.
Повний текст джерела