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



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


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


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


A Mouse Model For Celiac Disease


The immunopathogenic  mechanisms in Celiac Disease

In vivo models of intestinal gluten sensitivity

Recent advances


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



Arterial injury

Vein graft atherosclerosis

Transplant arteriosclerosis





Disease Models by Leukocyte-specific mutagenesis in Mice



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


The Immunological Disease Continuum- Implications for animal models