The Rose and Mackay textbook of autoimmune diseases /

**Selected for 2025 Doody's Core TitlesĀ® with "Essential Purchase" designation in Allergy/Clinical Immunology**The Rose-Mackay Textbook of Autoimmune Diseases, Seventh Edition is a comprehensive reference that emphasizes the "3 P's" of 21st Century medicine: precision,...

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Bibliographic Details
Corporate Author: ScienceDirect (Online service)
Other Authors: Gershwin, M. Eric, 1946- (Editor), Tsokos, George C. (Editor), Diamond, Betty (Editor)
Format: eBook
Language:English
Published: [Place of publication not identified] : Academic Press, 2024.
Edition:Seventh edition.
Subjects:
Online Access:Connect to the full text of this electronic book
Table of Contents:
  • 9780443239472v1_WEB
  • Front Cover
  • The Rose and Mackay Textbook of Autoimmune Diseases
  • Copyright Page
  • Dedication
  • Contents to Volume 1
  • List of contributors
  • List of editors and section editors
  • Editors
  • Section editors
  • Basic science
  • Ear nose and throat
  • Dermatology
  • Endocrinology
  • Hematology
  • Hepatobiliary and gastroenterology
  • Nephrology
  • Neurology
  • Ophthalmology
  • Pulmonary
  • Rheumatology
  • Preface
  • 1 Basic science: development of the immune system with cell lineages
  • 1. Development of adaptive immune cells
  • Self versus nonself
  • Adaptive immune cell development
  • Lymphocyte progenitors
  • T cell development
  • Altered mechanisms of T cell tolerance as promoters of autoimmunity
  • B cell development
  • Antibody diversity
  • Self-reactive B cells are inherently part of the peripheral B cell pool
  • Altered mechanisms of B cell tolerance and autoimmunity
  • Conclusion
  • Acknowledgment
  • References
  • 2. Revision to the origins of the mononuclear phagocyte
  • Key points
  • Overview
  • Steady-state development of macrophages
  • Transcriptional regulation of tissue-resident macrophages
  • Common macrophage transcriptional profiles
  • Adipose tissue macrophages
  • Cardiac tissue macrophages
  • Intestinal macrophages
  • Kupffer cells
  • Langerhans cells
  • Peritoneal macrophages
  • Lung macrophages
  • Brain macrophages
  • Nerve-associated macrophages
  • Osteoclasts
  • Splenic macrophages
  • Synovial macrophages
  • M1 and M2 paradigm revisited
  • Future directions
  • References
  • 3. Tolerance and activation of peripheral B and T cells
  • B cell central tolerance "checkpoints" in humans
  • Tonic signaling at the immature B cell stage
  • Receptor editing is likely a dominant tolerance mechanism at the immature B cell stage in mice and humans.
  • The special case of immature B cell deletion in response to DNA-protein complexes
  • T cell activation, T-B collaboration, and peripheral B cell tolerance
  • Self-reactive B cells at the transitional B cell stages are likely most susceptible to receptor downregulation and subseque...
  • Late transitional and mature follicular B cells are anergized by selective downregulation of IgM, but anergic B cells are a...
  • An overview of T cell tolerance and peripheral T cell activation
  • The simultaneous generation of CD4+ T cell subsets and the induction of the extrafollicular response
  • The transient extrafollicular induction of autoimmunity after infection likely reflects the major contribution of self-reac...
  • The extrafollicular response, tolerance, and common autoimmune disorders
  • Regulatory T cells in the maintenance of B cell tolerance
  • Autoantibodies in common variable immunodeficiency likely reflect altered T effector/T reg ratios that allow anergic B cell...
  • Germinal center B cell tolerance may reflect a default process and a break in tolerance at this location may lead to frank ...
  • Conclusion
  • Acknowledgments
  • References
  • 4. Genetic alterations leading to autoimmunity
  • Introduction
  • The genetics of autoimmunity before development of the genome-wide association study
  • Evidence supporting the role of genetics in autoimmune diseases
  • Linkage studies in autoimmune diseases
  • Candidate gene studies identify the first non-HLA associated autoimmune disease risk genes
  • The genome-wide association study
  • Genome-wide association study discover a trove of autoimmune disease associations
  • Fine mapping autoimmune disease loci with the Immunochip
  • Moving from genetic association to functional mechanism in the post-GWAS era
  • The next technology advance: single cell sequencing.
  • Leveraging polygenic risk scores to predict disease
  • Summary
  • References
  • 5. Microbiome in autoimmunity
  • Introduction
  • Alterations in the gut microbiome in autoimmune diseases
  • Inflammatory bowel diseases
  • Type 1 diabetes
  • Multiple sclerosis
  • Rheumatoid arthritis
  • Systemic lupus erythematosus
  • Mechanisms
  • Metabolites
  • Molecules mimicry
  • Microbiota translocation
  • Interventions
  • Diet and metabolites
  • Fecal microbiota transplantation
  • Inflammatory bowel diseases
  • Type 1 diabetes
  • Multiple sclerosis
  • Rheumatoid arthritis
  • Systemic lupus erythematosus
  • Conclusion
  • References
  • 6. Metabolic control of pathogenesis in autoimmune diseases
  • Short summary
  • Introduction
  • Systemic lupus erythematosus
  • Mitochondrial oxidative stress underlies mTOR activation in SLE
  • Rheumatoid arthritis
  • Autoimmune spondyloarthritis
  • Scleroderma and systemic sclerosis
  • Metabolic control of organ-specific autoimmune diseases
  • Conclusions
  • Acknowledgments
  • References
  • 7. Triggers for autoimmunity
  • Introduction
  • Self-antigens that escape tolerance
  • Neoantigens
  • Breaking tolerance to existing autoantigens
  • Enhanced presentation of posttranslationally modified epitopes
  • Cryptic epitopes
  • Sequestered antigens
  • Environmental triggers of autoimmunity
  • Viral-induced autoimmunity
  • Epstein-Barr virus
  • Enterovirus
  • Hepatitis C virus
  • Herpes simplex virus
  • SARS-CoV-2
  • Drug-induced autoimmunity
  • Drug-induced lupus
  • Potential mechanisms of drug-induced lupus
  • Cellular autoimmunity
  • Neutrophil extracellular traps
  • Immune checkpoint inhibitor-induced autoimmunity
  • Potential mechanisms of immune checkpoint inhibitor-induced autoimmunity
  • Cellular autoimmunity
  • Humoral autoimmunity
  • Cytokine production
  • Conclusion
  • References
  • 8. Organ damage in autoimmune disease.
  • Introduction
  • Initiation of tissue injury
  • Antibody-mediated tissue injury
  • Organ-specific diseases initiated by autoantibodies
  • Autoantibodies of unknown function
  • Antibodies directed at ubiquitous self-antigens
  • B cells as organizers of local inflammation
  • B cell-directed therapies
  • T cell-mediated tissue injury
  • T cells as inflammatory effector cells
  • Antigen-specific T cells
  • T cells as B cell helpers or regulatory cells
  • T cell-directed therapies
  • Innate immune mechanisms
  • Macrophages
  • Neutrophils
  • Innate lymphoid cells
  • Soluble inflammatory mediators
  • Soluble mediators of resolution
  • Chronic tissue injury
  • Hypoxia
  • Immune senescence
  • Cell death
  • Fibrosis
  • Fibroblasts
  • Pro-fibrotic and antifibrotic soluble mediators
  • Targeting fibrosis
  • Failed resolution
  • Genetics of tissue injury
  • Loss of function
  • Implications for therapy
  • References
  • 9. Therapeutic strategies for treating autoimmune disease
  • Immunosuppression versus targeted therapy
  • B cell depletion
  • T cell-directed therapy
  • Cytokine blockade
  • Small molecule immune inhibitors
  • Immunoablation and reconstitution
  • Antigen-specific therapy
  • Conclusion
  • References
  • 2 Rheumatology
  • 10. Systemic lupus erythematosus
  • Introduction
  • History
  • Disease diagnosis and classification
  • Epidemiology, genetics, and the environment
  • Pathogenesis
  • Adaptive immunity
  • Innate immunity
  • Clinical features
  • Clinical presentation
  • Mucocutaneous manifestations
  • Arthritis
  • Renal involvement
  • Neuro-psychiatric disease
  • Hematologic manifestations
  • Pulmonary and cardiovascular manifestations
  • Other clinical manifestations
  • Infections
  • Clinical laboratory findings
  • Treatment
  • Outcome measures
  • General therapeutic schema
  • Therapeutic agents
  • Antimalarials
  • Corticosteroids
  • Biologics.
  • Immunosuppressive medications
  • Calcineurin inhibitors
  • Cyclophosphamide
  • Supportive treatments
  • Future directions
  • References
  • 11. Systemic sclerosis (scleroderma)
  • Definition and classification
  • Epidemiology and etiology
  • Sex bias, ethnic background and mortality trends
  • Environmental factors
  • Pathogenesis
  • Genetic associations
  • Preclinical disease models
  • Microvascular disease in systemic sclerosis
  • Inflammation and autoimmunity
  • Cellular immunity
  • Humoral autoimmunity
  • Fibrosis
  • Pathology
  • Skin
  • Lungs
  • Gastrointestinal tract
  • Kidneys
  • Heart
  • Pathology in other organs
  • Clinical features
  • Overview
  • Initial clinical presentation
  • Organ involvement
  • Raynaud's phenomenon
  • Skin features
  • Pulmonary features
  • Interstitial lung disease
  • Gastrointestinal involvement
  • Renal involvement: scleroderma renal crisis
  • Cardiac involvement
  • Musculoskeletal complications
  • Less recognized disease manifestations
  • Biomarkers and autoantibodies in systemic sclerosis
  • Screening and follow-up evaluation
  • Management of patients with systemic sclerosis
  • General principles
  • Disease-modifying immunomodulatory therapy
  • Therapy targeting fibrosis
  • Vascular therapy
  • Treatment of gastrointestinal complications
  • Treatment of interstitial lung disease
  • Management of renal crisis
  • Treatment of pulmonary arterial hypertension
  • Natural history and prognosis
  • References
  • 12. Antiphospholipid syndrome
  • Historical perspective
  • Geoepidemiology
  • Pathogenesis
  • Double-hit model
  • Thrombosis
  • Activation of endothelial cells, platelets and immune cells
  • Complement activation
  • Resistance to activated protein C
  • Pregnancy complications
  • Proliferation and migration of trophoblasts
  • Inflammation
  • Complement activation
  • Genetics
  • Diagnosis, screening, and prevention.