Targeted pancreatic β-cell destruction by activated immune cells is a hallmark of type 1 diabetes in human beings and rodents. Activated T-lymphocytes, B-lymphocytes and antigen presenting cells all migrate to the pancreatic islets and orchestrate a β-cell specific inflammatory immune response. While the timing and sequence of these invading, migratory cell populations are undoubtedly critical and fundamental to our understanding of this disease, many details of the process are still poorly understood. Here, we review our present knowledge of immune cell trafficking, adhesion molecules and matrix interactions as they relate to the pathogenesis of type 1 diabetes. Understanding the roles that adhesion molecules play in guiding the flux of immune cell populations between the pancreatic islets, the vascular endothelium, the pancreatic lymph nodes and other lymphoid tissues will provide us with new therapeutic targets for type 1 diabetes and insights into the pathogenesis of the disease.
Keywords: Type 1 diabetes, NOD mice, adhesion molecules, chemokines, matrix, integrins
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