Journal
ENDOCRINE JOURNAL
Volume 57, Issue 11, Pages 991-996Publisher
JAPAN ENDOCRINE SOC
DOI: 10.1507/endocrj.K10E-076
Keywords
Biopsy; Chemokine; IP-10; CXCL10; CXCR3
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Funding
- Japanese Society for the Promotion of Science [KAKENHI 19790641, 19591087, 19591069]
- Naito Foundation
- Takeda Science Foundation
- Japanese Ministry of Health, Labour and Welfare
- Grants-in-Aid for Scientific Research [19591087, 19591069] Funding Source: KAKEN
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The aim of this study is to present direct evidence for the involvement of CXC chemokine ligand 10 (CXCL10) and CXCR3 in human autoimmune type 1 diabetes. We examined five patients with recent-onset type 1 diabetes and five control subjects without diabetes. Islet cell antibodies or GAD antibodies or both were detected in all five patients. We used double-immunofluorescence to detect the expression of CXCL10 and CXCR3 (the receptor of CXCL10). CXCL10 was detected in the islets of all five patients. Almost all (84.2 +/- 10.3 %, mean +/- SD) CXCL10-positive cells were insulin-positive in the islet area. CXCL10-positive cells with glucagons, somatostatins or pancreatic polypeptides were not detected at all. CXCL10 expression was not seen in any islet without beta cells. CXCR3 was detected in the islet areas of all five patients. Almost all (80.3 +/- 13.4 %, mean +/- SD) CXCR3-positive cells were CD3-positive T cells. Our study showed that CXCL10 was expressed in the remaining beta cells, and the infiltrating T cells expressed CXCR3, in pancreatic islets of patients with recent-onset type 1 diabetes. The interaction of CXCL10 and CXCR3 would contribute to the selective destruction of beta cells in the development of type 1 diabetes.
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