Ankylosing spondylitis - Axial spondyloarthritis : cellular, molecular and environmental factors / / edited by Mohammad Hossein Nicknam

• Pubblicazione: Gateway East, Singapore : , : Springer, , [2022]; ©2022
• Descrizione fisica: 1 online resource (188 pages)
• Disciplina: 616.73
• Soggetto topico: Ankylosing spondylitis - Molecular aspects; Ankylosing spondylitis; Spondylitis, Ankylosing; Espondiloartritis anquilosant
• Soggetto genere / forma: Llibres electrònics
• Persona (resp. second.): NicknamMohammad Hossein
• Nota di bibliografia: Includes bibliographical references and index.
• Nota di contenuto: Intro -- Preface -- Contents -- About the Editor -- Part I: Introduction -- 1: An Overview to Ankylosing Spondylitis and Spondyloarthropathies -- 1.1 History -- 1.2 Epidemiology -- 1.3 Clinical Manifestation -- 1.3.1 General Symptoms, Spondylitis and Arthritis -- 1.3.2 Extra-Articular Manifestations -- 1.3.3 Complications and Co-morbidities -- 1.4 Diagnosis -- 1.4.1 History and Physical Examination -- 1.4.2 Lab Test -- 1.4.3 Imaging -- 1.4.3.1 Plain Radiography -- 1.4.3.2 Computed Tomography -- 1.4.3.3 Magnetic Resonance Imaging -- 1.4.4 Classification and Diagnostic Criteria -- 1.5 Pathogenesis -- 1.6 Treatment -- 1.6.1 Nonsteroidal Anti-Inflammatory Drugs -- 1.6.2 Glucocorticoids -- 1.6.3 Disease-Modifying Anti-Rheumatic Drugs -- 1.7 Conclusion -- References -- Part II: Cells and Cytokines -- 2: Innate Immune-Related Cells and Cytokines in Spondyloarthropathies -- 2.1 Introduction -- 2.2 Innate Immunity Components -- 2.2.1 Pattern Recognition Receptors (PRR) -- 2.2.1.1 Toll-Like Receptors (TLRs) -- 2.2.1.2 NOD-Like Receptors (NLRs) -- 2.2.2 Innate Cytokines -- 2.2.2.1 IL-1 Family -- 2.2.2.1.1 IL-1 and Receptors -- 2.2.2.1.2 IL-37 -- 2.2.2.2 TNF and Receptors -- 2.2.2.3 IL-23 and Receptor -- 2.2.3 Soluble Components of Innate Immunity -- 2.2.3.1 Defensins -- 2.2.3.2 Complement System -- 2.2.4 Innate Immune Cells -- 2.2.4.1 Dendritic Cells (DC) -- 2.2.4.2 Macrophage Cells -- 2.2.4.3 Natural Killer (NK) Cells -- References -- 3: Adaptive Immune-Related Cells and Cytokines in Spondyloarthropathies -- 3.1 Adaptive immunity in autoimmune disorders -- 3.2 The Pathogenic Role of Adaptive Immune Lymphocytes in SpAs -- 3.3 T Cell Activation, Signaling, and Cytokines in SpAs -- 3.3.1 Th1 and Th2 role in SpAs -- 3.3.2 Th17 and IL-17 in SpAs -- 3.3.2.1 IL-17 and Enthesitis -- 3.3.2.2 IL-17 and Bone Remodeling. ; 3.3.2.3 Targeting Th17 in SpAs -- 3.3.3 Th22 and IL-22 in SpAs -- 3.3.4 Functional Abnormalities of Regulatory T Cells in SpAs -- 3.3.5 Cytotoxic T Cell in SpAs -- 3.3.6 Gamma Delta T Cells and SpAs -- 3.4 B Cell Activation and Signaling -- 3.5 Conclusions and Future Directions -- References -- Part III: Genes -- 4: Association of HLA and HLA-Related Genes with Ankylosing Spondylitis -- 4.1 Biology of HLA Expression and Functions -- 4.1.1 Genomic Organization -- 4.1.1.1 HLA Nomenclature -- 4.1.2 Molecular Structure -- 4.1.2.1 Molecular Structure of HLA-Class I -- 4.1.2.2 Molecular Structure of HLA-Class II -- 4.1.3 Pathways of Antigen Presentation -- 4.1.3.1 Processing and Presentation of Endocytosed Antigens -- 4.1.3.2 Processing and Presentation of Cytosolic Antigens -- 4.2 Association of HLA loci with Ankylosing Spondylitis -- 4.2.1 HLA-B27 -- 4.2.1.1 Arthritogenic Peptide Hypothesis -- 4.2.1.2 HLA-B27 Misfolding Hypothesis -- 4.2.1.3 HLA-B27 Dimer Hypothesis -- 4.2.2 HLA Genes Other Than HLA-B27 -- 4.3 Association of HLA-Related Genes with Ankylosing Spondylitis -- 4.3.1 Transporters in Antigen Presenting (TAP) -- 4.3.2 M1 zinc-Aminopeptidases -- 4.3.2.1 Endoplasmic Reticulum Aminopeptidase (ERAP)-1 -- 4.3.2.2 ERAP2 -- 4.3.2.3 NPEPPS -- 4.3.2.4 Ubiquitinases -- 4.3.2.5 LMP2 -- 4.4 Role of Epigenetics in Ankylosing Spondylitis Pathogenesis -- 4.4.1 DNA Methylation -- 4.4.2 Histone Modifications -- 4.4.3 MicroRNAs -- References -- 5: Association of Non-HLA Genes with Ankylosing Spondylitis -- 5.1 Cytokines and Cytokine-Receptors -- 5.1.1 IL-1RN Gene -- 5.1.2 IL-6 Receptor Gene -- 5.1.3 IL-12B Gene -- 5.1.4 IL-17 Gene -- 5.1.5 IL-23 and IL-23 Receptor -- 5.1.6 TNF and TNF Receptor -- 5.1.7 IL-10 Gene -- 5.2 Overview on Signal Transduction -- 5.2.1 VDR Gene -- 5.2.2 TLR4 Gene. ; 5.2.3 G Protein-Coupled Receptor Gene -- 5.2.4 CTLA-4 Gene -- 5.2.5 PD-1 Gene -- 5.2.6 PTPN22 Gene -- 5.2.7 CARD9 Gene -- 5.2.8 TBKBP1 Gene -- 5.2.9 TRADD Gene -- 5.2.10 STAT3 Gene -- 5.2.11 STAT4 Gene -- 5.2.12 RUNX3 Gene -- 5.2.13 TBX21 Gene -- 5.2.14 Ancillary Mediators Involved in Lymphocyte Differentiation -- 5.3 Other Associated Genes with AS Disease -- 5.3.1 ANTXR2 -- 5.3.2 SNAPC4 -- 5.3.3 KIF21B -- 5.3.4 PTGER4 -- 5.3.5 PPARGC1B -- 5.3.6 ANO6 Gene -- 5.3.7 Β-Defensin Gene Clusters -- 5.3.8 Pentraxin3 -- 5.3.9 MIF Gene -- 5.3.10 BCL11B -- 5.3.11 Autophagy-Related Genes -- References -- Part IV: Environmental Factors -- 6: Spondyloarthropathies and Gut Microbiota -- 6.1 Introduction -- 6.2 Gut Microbiome -- 6.3 Spondyloarthropathies and Microbes -- 6.4 Spondyloarthropathies and Inflammatory Bowel Diseases -- 6.5 Animal Models of SpA and Gut Immunity -- 6.6 Dysbiosis and Inflammation in SpA -- 6.7 HLA-B27 -- 6.8 Cytokines Induction by Microbiome -- 6.9 Probiotics and Prebiotics -- 6.10 Antibiotics and Fecal Transplant -- 6.11 Conclusion -- References -- 7: Spondyloarthropathies and Food Intake -- 7.1 Introduction -- 7.1.1 Spondyloarthropathies -- 7.1.2 Ankylosing Spondylitis -- 7.2 Vitamins -- 7.2.1 Vitamin D -- 7.2.2 Other Vitamins -- 7.2.2.1 Vitamin E -- 7.2.2.2 Vitamin A -- 7.3 Low Starch Diet and Klebsiella -- 7.4 Fatty Acids -- 7.5 Obesity -- 7.6 Food Allergy -- 7.7 Conclusion -- References -- 8: Spondyloarthropathies and Environmental Stresses -- 8.1 Introduction -- 8.2 Biomechanical Stress -- 8.3 Psychological Stress -- 8.4 Oxidative Stress -- 8.5 Smoking -- 8.6 Vaccination -- References -- Index.
• Titolo autorizzato: Ankylosing spondylitis - Axial spondyloarthritis
• ISBN: 981-16-4733-X; 981-16-4732-1
• Formato: Materiale a stampa
• Livello bibliografico: Monografia
• Lingua di pubblicazione: Inglese
• Record Nr.: 9910743382103321
• Lo trovi qui: Univ. Federico II