Differential Expression of CC Chemokines and the CCR5 Receptor in the Pancreas Is Associated with Progression to Type I Diabetes
作者： Mark J. Cameron , Guillermo A. Arreaza , Marsha Grattan , Craig Meagher , Shayan Sharif
DOI: 10.4049/JIMMUNOL.165.2.1102
关键词: Chemokine receptor 、 Insulitis 、 Biology 、 Internal medicine 、 Pancreas 、 Nod 、 Chemokine receptor CCR5 、 Immunology 、 Monocyte 、 Diabetes mellitus 、 NOD mice 、 Endocrinology
摘要: We investigated the biological role of CC chemokines in Th1-mediated pathogenesis spontaneous type I diabetes nonobese diabetic (NOD) mice. Whereas an elevated ratio macrophage inflammatory protein-1α (MIP-1α):MIP-1β pancreas correlated with destructive insulitis and progression to NOD mice, a decreased intrapancreatic MIP-1α:MIP-1β was observed diabetes-resistant (NOR) IL-4 treatment, which prevents mice by polarizing intraislet Th2 responses, CCR5 expression islets potentiated high MIP-1β monocyte chemotactic protein-1 (MCP-1): MIP-1α pancreas. Furthermore, NOD.MIP-1α−/− exhibited reduced were protected from diabetes. Neutralization specific Abs following transfer diabetogenic T cells delayed onset NOD. Scid recipients. These studies illustrate that temporal certain chemokines, particularly MIP-1α, chemokine receptor is associated development
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