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Auswahl der wissenschaftlichen Literatur zum Thema „Immunte tolerance breakdown“
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Zeitschriftenartikel zum Thema "Immunte tolerance breakdown"
Bird, Lucy. „NKT cells linked to immune tolerance breakdown“. Nature Reviews Immunology 8, Nr. 7 (Juli 2008): 493. http://dx.doi.org/10.1038/nri2370.
Der volle Inhalt der QuelleHampe, Christiane S., und Hiroshi Mitoma. „A Breakdown of Immune Tolerance in the Cerebellum“. Brain Sciences 12, Nr. 3 (28.02.2022): 328. http://dx.doi.org/10.3390/brainsci12030328.
Der volle Inhalt der QuelleEmmanuel K, Mugisha. „Adaptive Immunity and Autoimmune Disease: Mechanisms, Pathogenesis, and Therapeutic Approaches“. NEWPORT INTERNATIONAL JOURNAL OF BIOLOGICAL AND APPLIED SCIENCES 5, Nr. 3 (01.12.2024): 44–48. https://doi.org/10.59298/nijbas/2024/5.3.444811.
Der volle Inhalt der QuelleKamyshny, Alex, Denis Putilin und Vita Kamyshna. „BREAKDOWN IN PERIPHERAL IMMUNE TOLERANCE IN EXPERIMENTAL DIABETES MELLITUS“. Journal of Molecular Pathophysiology 5, Nr. 3 (2016): 31. http://dx.doi.org/10.5455/jmp.20160609022446.
Der volle Inhalt der QuelleCheng, Mickie, und Lawrence Nelson. „Mechanisms and Models of Immune Tolerance Breakdown in the Ovary“. Seminars in Reproductive Medicine 29, Nr. 04 (Juli 2011): 308–16. http://dx.doi.org/10.1055/s-0031-1280916.
Der volle Inhalt der QuelleBukhari, Shoiab, Aaron F. Mertz und Shruti Naik. „Eavesdropping on the conversation between immune cells and the skin epithelium“. International Immunology 31, Nr. 7 (05.02.2019): 415–22. http://dx.doi.org/10.1093/intimm/dxy088.
Der volle Inhalt der QuellePeter, Elise, Isabelle Treilleux, Valentin Wucher, Emma Jougla, Alberto Vogrig, Daniel Pissaloux, Sandrine Paindavoine et al. „Immune and Genetic Signatures of Breast Carcinomas Triggering Anti-Yo–Associated Paraneoplastic Cerebellar Degeneration“. Neurology - Neuroimmunology Neuroinflammation 9, Nr. 5 (12.07.2022): e200015. http://dx.doi.org/10.1212/nxi.0000000000200015.
Der volle Inhalt der QuelleJones, DEJ, JM Palmer, AJ Robe, MH Bone, AD Burt, SJ Yeaman, JA Kirby und MF Bassendine. „A Novel Mechanism of Immune Tolerance Breakdown and Autoimmune Disease Induction“. Clinical Science 100, s44 (01.02.2001): 13P. http://dx.doi.org/10.1042/cs100013pb.
Der volle Inhalt der QuelleLiao, Xiaofeng, Alec M. Reihl und Xin M. Luo. „Breakdown of Immune Tolerance in Systemic Lupus Erythematosus by Dendritic Cells“. Journal of Immunology Research 2016 (2016): 1–15. http://dx.doi.org/10.1155/2016/6269157.
Der volle Inhalt der QuelleP. Singh, Ram, David S. Bischoff, Satendra S Singh und Bevra H. Hahn. „Peptide-based immunotherapy in lupus: Where are we now?“ Rheumatology and Immunology Research 4, Nr. 3 (01.09.2023): 139–49. http://dx.doi.org/10.2478/rir-2023-0020.
Der volle Inhalt der QuelleDissertationen zum Thema "Immunte tolerance breakdown"
Villagrán-García, Macarena. „Clinical-immunological characterization and immune tolerance breakdown in paraneoplastic neurological syndromes associated with Hu antibodies“. Electronic Thesis or Diss., Lyon 1, 2024. http://www.theses.fr/2024LYO10259.
Der volle Inhalt der QuelleHu antibodies, the most common in paraneoplastic neurological syndromes (PNS), strongly indicate small-cell lung cancer (SCLC). The clinical spectrum of Hu-PNS is diverse, most patients develop multifocal central, peripheral, and/or autonomic nervous system dysfunction. Despite extensive research, questions remain, namely regarding the immunological basis of clinical heterogeneity and why only a minority of SCLC patients develop Hu-PNS. Our PhD project aims to phenotype Hu-PNS patients, explore the immunogenetics and humoral responses underlying neurological phenotypes, and the genomic and transcriptomic features of their SCLC. First, we described 466 Hu-PNS patients. Hierarchical clustering identified three groups: patients with central nervous system (CNS) involvement; isolated neuropathy; and mixed CNS/peripheral phenotypes. Overall survival was similar across groups, primarily determined by cancer, but dysautonomia, present in 26% of patients, significantly influenced neurological mortality. Prominent CNS dysfunction led to fatal cardiovascular dysautonomia or central hypoventilation, while peripheral involvement was associated with gastrointestinal or secretomotor alterations, without increased mortality risk. We also characterized patients who developed neurological syndromes with Hu antibodies after immune checkpoint inhibitor (ICI) treatment. These patients were clinically indistinguishable from spontaneous cases and shared a strong association with SCLC, suggesting ICIs may induce Hu-PNS. Second, we immunologically investigated neurological phenotypes using two approaches. HLA genotyping of 100 patients confirmed an association with the DR3~DQ2 haplotype, particularly in patients with sensory neuropathy, and absent in those with only CNS involvement. Phage immunoprecipitation sequencing was used to evaluate Hu antibody epitope reactivity and other autoantibodies in serum and/or CSF of 210 patients. We found no direct clinical association with the Hu dominant epitope, but epitope reactivity differed between serum and CSF in 75% of patients with paired samples. This variation correlated with sample timing and phenotype: CSF from patients with differing serum/CSF epitopes was collected later after PNS onset, while patients with serum/CSF consistent epitope reactivity always had CNS phenotypes. In addition, we identified reactivities to other proteins, some more specific to serum or CSF, and a subset linked to specific phenotypes. Third, we examined SCLC molecular features of Hu-, GABAbR-PNS and control patients. Next-generation sequencing, copy number variation analysis, and bulk-RNA sequencing revealed no mutations, gains, deletions, or overexpression in the Hu gene family of Hu-PNS SCLC. However, a distinct transcriptomic profile with upregulated genes largely related to immune system processes characterized these tumors. We also identified specific genes upregulated in the SCLC of patients with sensory neuropathy, some of which were linked to axonogenesis and neuropathy development. Our findings suggest multiple factors contribute to Hu-PNS clinical variability, particularly a broad range of additional autoantigens. These may be partly driven by gene expression patterns in SCLC, as some upregulated genes in patients with sensory neuropathy were linked to axonogenesis. Genetic predisposition may also favor specific phenotypes, as the DR3~DQ2 haplotype was associated with sensory neuropathy. Compartmentalization within the nervous system could further contribute, as most patients targeted different Hu epitopes in serum and CSF, and some autoantigens were more specific to CSF. Finally, Hu genes alterations in SCLC are unlikely causes of neoantigenicity, while a distinct immune-related gene profile and ICIs could contribute to immune tolerance breakdown. This work advances understanding of Hu-PNS complexity and paves the way for further studies into the immunological and molecular drivers of paraneoplastic immunity
Robe, Amanda Jane. „Investigation of the breakdown of immune tolerance to pyruvate dehydrogenase complex (PDC)“. Thesis, University of Newcastle Upon Tyne, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.413949.
Der volle Inhalt der QuelleBuchteile zum Thema "Immunte tolerance breakdown"
Giardino, Giuliana, Emilia Cirillo, Rosaria Prencipe, Roberta Romano, Francesca Cillo, Elisabetta Toriello, Veronica De Rosa und Claudio Pignata. „Mechanisms of immune tolerance breakdown in inborn errors of immunity“. In Translational Autoimmunity, 73–95. Elsevier, 2022. http://dx.doi.org/10.1016/b978-0-323-85415-3.00019-2.
Der volle Inhalt der QuelleSimmonds, Matthew J., und Stephen C. L. Gough. „Endocrine autoimmunity“. In Oxford Textbook of Endocrinology and Diabetes, 34–44. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199235292.003.1031.
Der volle Inhalt der QuelleChatham, W. Winn, Jeffrey C. Edberg, und Robert P. Kimberly. „The Role Of Neutrophils In The Pathogenesis Of Rheumatoid Arthritis“. In Rheumatoid Arthritis, 95–106. Oxford University PressOxford, 2006. http://dx.doi.org/10.1093/oso/9780198566304.003.0007.
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