Proceedings from the February 2nd 2007 meeting in London, UK
“The main goal of this meeting was to get together clinical and basic immunologists trying to gather insights into the pathogenic mechanisms of human diseases and immunotherapy. Due to the limitations of the human system, these investigations often rely on the use of animal models developing spontaneous diseases. In this meeting we evaluated the pros and cons of some of the most used and valuable animal models of disease and some new models, which will open new therapeutic ways to treat human diseases”. Dr Sonia Quaratino, Reader in Immunology, Cancer Research UK Clinical Centre, University of Southampton
This meeting was chaired by: Dr Sonia Quaratino, Reader in Immunology, Cancer Research UK Clinical Centre, University of Southampton
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Table of Contents
Preface
Contents
Why use spontaneous models of human disease?
Biological processes in complex organisms, especially mammals, have many features in common
Many pathological processes in humans are very complex, and as populations are outbred
Some ‘artificial’ models provide information about ‘natural’ regulatory mechanisms for potential therapeutic use
A novel humanized animal model of spontaneous autoimmune thyroiditis
References
Understanding the Pathogenesis and Treatment of Multiple Sclerosis Through Experimental Models
Humanized, spontaneous transgenic models of MS – immunology, imaging and therapeutics
Spontaneous And Induced Models Of Rheumatoid Arthritis
Introduction
Models of arthritis induced by immunization
Adjuvant arthritis
Antigen-induced arthritis
Streptococcal cell wall-induced arthritis
Collagen-induced arthritis (CIA)
Proteoglycan-induced arthritis
Cartilage oligomeric matrix protein-induced arthritis
Spontaneous arthritis in transgenic strains of mice
hTNF transgenic mice
hIL-1a transgenic mice
The KRN model of arthritis
References
A Mouse Model For Celiac Disease
Abstract
The immunopathogenic mechanisms in Celiac Disease
In vivo models of intestinal gluten sensitivity
Recent advances
References1
The myodystrophy mouse; providing insights into the glycobiology of muscular dystrophy
What have we learned from spontaneous animal models of muscular dystrophy
Mouse Models of Arteriosclerosis
Abstract
Introduction
Arterial injury
Vein graft atherosclerosis
Transplant arteriosclerosis
Limitation
Perspectives
Acknowledgements
References
Disease Models by Leukocyte-specific mutagenesis in Mice
Abstract
Introduction
Csk-deficiency in granulocytes leads to acute inflammatory disease
B cell specific inactivation of the TGF-b receptor causes IgA deficiency, B cell hyperplasia and hyper-g-globulinaemia
Tracking homeostatic pathways and mediators in primary cells
References
The Immunological Disease Continuum- Implications for animal models
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