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The Value of BCG and TNF in Autoimmunity provides an overview of current research and thinking related to tumor necrosis factor (TNF) induction and the use of the bacillus Calme… Read more
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Immediately download your ebook while waiting for your print delivery. No promo code needed.
The Value of BCG and TNF in Autoimmunity provides an overview of current research and thinking related to tumor necrosis factor (TNF) induction and the use of the bacillus Calmette-Guérin (BCG) vaccine as potential treatment approaches to diverse forms of autoimmunity. BCG, commonly known as an anti-tuberculosis vaccine, is being explored in worldwide clinical trials as an approach to the treatment of certain forms of autoimmunity. The scope of research behind this therapeutic approach spans from the basic science of TNF signaling to research in diverse autoimmune disciplines, such as type 1 diabetes and multiple sclerosis.
Overall, the book focuses on the lessons that can be learned from the researchers' individual experiences and data, and provides a rationale for bringing the inexpensive, generic BCG vaccine to the forefront of clinical trials in different forms of autoimmunity.
Clinical researchers and scientists working in the fields of autoimmunity and/or immunology
Chapter 1. Mycobacteria, Immunoregulation, and Autoimmunity
Chapter 2. Prevention of Type 1 Diabetes and Its Recurrence by Immunotherapy with Mycobacterial Adjuvants
Chapter 3. Proteasome Defects and Cytokine Signaling in Sjögren’s Syndrome
Chapter 4. The Protective Effect of the BCG Vaccine on the Development of Type 1 Diabetes in Humans
Chapter 5. Effects of the Bacillus Calmette-Guérin (BCG) Vaccine in the Demyelinating Disease of the Central Nervous System
Chapter 6. TNF, BCG, and the Proteasome in Autoimmunity: An Overview of the Pathways & Results of a Phase I Study in Type 1 Diabetes
Chapter 7. Why Test BCG in Sjögren’s Syndrome?
Chapter 8. Celiac Disease as a Model Disorder for Testing Novel Autoimmune Therapeutics
Chapter 9. Delivering Solutions and Clinical Benefits for Diseases with Small and Intermediate-Size Patient Populations
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Denise L. Faustman, MD, PhD, is Director of the Immunobiology Laboratory at the Massachusetts General Hospital (MGH) and an Associate Professor of Medicine at Harvard Medical School. She has worked in the field of autoimmunity for nearly two decades. In 2001, the Faustman Lab reversed type 1 diabetes in mice with end-stage disease, a project that is now in human clinical trials. Dr. Faustman’s current research is focused on uncovering new treatments for type 1 diabetes, as well as searching for therapies for other autoimmune diseases, including Crohn's disease, lupus, scleroderma, rheumatoid arthritis, Sjögren's syndrome, and multiple sclerosis.
Dr. Faustman’s earlier research achievements include key discoveries regarding the role of MHC Class I antigen presentation in immunity and introducing the concept of modifying antigens on donor tissues to prevent their rejection. After completing her internship, residency, and fellowships in Internal Medicine and Endocrinology at the MGH, Dr. Faustman became an independent investigator at the MGH and Harvard Medical School in 1987. She is a member of the American Association for the Advancement of Science (AAAS) and serves as a frequent member of the Institute of Medicine in Washington, DC.
Dr. Faustman's honors in recent years include:
Dr. Faustman is credited with the discovery of the role of CD8 T cells in type 1 diabetes, the discovery that HLA class I was an educational structure interrupted in self antigen presentation in autoimmunity, the discovery of first interruptions in the TNF and NFkB signaling pathway in autoimmunity in this case in the proteasome, the discovery that even end stage autoimmunity could be reversed in mice by the addition of TNF or TNF induction with BCG, the discovery of end organ pancreas regeneration in diseased animal models after BCG and more recently the discovery of functioning islet cells in the pancreas of the majority of human diabetics, decades after disease onset.