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Updated: Jun 17, 2026
06:27
Accelerated Type 1 Diabetes Induction in Mice by Adoptive Transfer of Diabetogenic CD4+ T Cells
Published on: May 6, 2013
Islet inflammation and CXCL10 in recent-onset type 1 diabetes.
B O Roep1, F S Kleijwegt, A G S van Halteren
1Department of Immunohaematology and Blood Transfusion, Leiden University Medical Center, Leiden, the Netherlands.
Clinical and Experimental Immunology
|January 12, 2010
Summary
Chemokine CXCL10 attracts T cells to pancreatic islets, driving inflammation and beta cell destruction in type 1 diabetes, irrespective of viral infection. This highlights CXCL10
Area of Science:
- Immunology
- Endocrinology
- Pathology
Background:
- Type 1 diabetes involves T cell destruction of pancreatic beta cells.
- Local factors influencing T cell migration to pancreatic tissue are poorly understood.
- Previous studies suggested viral infections in beta cells of type 1 diabetes patients.
Purpose of the Study:
- To investigate local factors contributing to T cell migration in type 1 diabetes.
- To analyze islet inflammation and T cell reactivity in recent-onset type 1 diabetes.
- To determine the role of chemokine CXCL10 and its receptor CXCR3 in insulitis.
Main Methods:
- Analysis of insulitis in pancreatic tissue from type 1 diabetes patients and controls.
- Measurement of chemokine CXCL10 and its receptor CXCR3 in pancreatic lesions.
- Study of T cell reactivity and cytokine patterns (IFN-gamma/IL-10) from draining lymph nodes.
Main Results:
- Insulitic lesions in type 1 diabetes patients showed elevated CXCL10 and CXCR3+ lymphocytes.
- CXCR3 and CXCL10 were absent in non-diabetic controls.
- T cells from a patient with viral infection exhibited reactivity to islet autoantigens and mixed cytokine profiles.
Conclusions:
- CXCL10 is a key cytokine in distressed islets, promoting insulitis and beta cell destruction, independent of viral infection.
- The findings suggest a significant role for CXCL10 in the pathogenesis of type 1 diabetes.
- Both pro- and anti-inflammatory autoimmune responses contribute to insulitis and beta cell destruction.
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