Abstract
The ability of the β-cells to control blood glucose levels depends on their function and mass. In both, type 1 and type 2 diabetes mellitus the main processes leading to β-cell failure are apoptosis and loss of function. Many studies demonstrate how cytokines and chemokines have an active role in triggering the immune-response against the β-cell population. In a recent study we have identified that the chemokine CXCL10 may play an active role in triggering β-cell destruction. We have identified the Toll like receptor 4 as the receptor for CXCL10 and as new pathway for the induction of β-cell apoptosis. Our findings may open new therapeutic approaches to fight onset and progression of the disease.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Apoptosis / genetics*
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Apoptosis / physiology
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Cell Death / genetics
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Cell Death / physiology
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Chemokine CXCL10 / genetics
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Chemokine CXCL10 / metabolism
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Chemokine CXCL10 / physiology*
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Diabetes Mellitus, Type 1 / genetics
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Diabetes Mellitus, Type 1 / pathology
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Diabetes Mellitus, Type 1 / physiopathology
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Diabetes Mellitus, Type 2 / genetics
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Diabetes Mellitus, Type 2 / pathology
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Diabetes Mellitus, Type 2 / physiopathology
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Humans
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Insulin-Secreting Cells / metabolism
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Insulin-Secreting Cells / physiology*
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Mice
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Models, Biological
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Toll-Like Receptor 4 / genetics
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Toll-Like Receptor 4 / metabolism
Substances
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Chemokine CXCL10
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Toll-Like Receptor 4