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*
Autoimmunity/Diabetes Group, The John P. Robarts Research Institute, London, Ontario, Canada;
Departments of Microbiology and Immunology, and Medicine, University of Western Ontario, London, Ontario, Canada;
Division of Pulmonary and Critical Care Medicine, University of Michigan Medical Center, University of Michigan, Ann Arbor, MI 48109; and
§
Department of Pathology, University of North Carolina School of Medicine, Chapel Hill, NC 27599
We investigated the biological role of CC chemokines in the
Th1-mediated pathogenesis of spontaneous type I diabetes in nonobese
diabetic (NOD) mice. Whereas an elevated ratio of macrophage
inflammatory protein-1
(MIP-1):MIP-1ß in the pancreas
correlated with destructive insulitis and progression to diabetes in
NOD mice, a decreased intrapancreatic MIP-1:MIP-1ß ratio was
observed in nonobese diabetes-resistant (NOR) mice. IL-4 treatment,
which prevents diabetes in NOD mice by polarizing intraislet Th2
responses, decreased CCR5 expression in islets and potentiated a high
ratio of MIP-1ß and monocyte chemotactic protein-1 (MCP-1): MIP-1
in the pancreas. Furthermore, NOD.MIP-1-/-
mice exhibited reduced destructive insulitis and were protected from
diabetes. Neutralization of MIP-1 with specific Abs following
transfer of diabetogenic T cells delayed the onset of diabetes in
NOD.Scid recipients. These studies illustrate that the
temporal expression of certain CC chemokines, particularly MIP-1,
and the CCR5 chemokine receptor in the pancreas is associated with the
development of insulitis and spontaneous type I
diabetes.
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