Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2014 Feb;25(1):57-65.
doi: 10.1016/j.cytogfr.2014.01.006. Epub 2014 Jan 28.

CXCR3, CXCL10 and type 1 diabetes

Alessandro Antonelli  1 , Silvia Martina Ferrari  2 , Alda Corrado  3 , Ele Ferrannini  4 , Poupak Fallahi  5
Affiliations
Review

CXCR3, CXCL10 and type 1 diabetes

Alessandro Antonelli et al. Cytokine Growth Factor Rev. 2014 Feb.

Abstract

Type 1 diabetes (T1D) is due to antigen-specific assaults on the insulin producing pancreatic β-cells by diabetogenic T-helper (Th)1 cells. (C-X-C motif) ligand (CXCL)10, an interferon-γ inducible Th1 chemokine, and its receptor, (C-X-C motif) receptor (CXCR)3, have an important role in different autoimmune diseases. High circulating CXCL10 levels were detected in new onset T1D patients, in association with a Th1 autoimmune response. Furthermore β-cells produce CXCL10, under the influence of Th1 cytokines, that suppresses their proliferation. Viral β-cells infections induce cytokines and CXCL10 expression, inducing insulin-producing cell failure in T1D. CXCL10/CXCR3 system plays a critical role in the autoimmune process and in β-cells destruction in T1D. Blocking CXCL10 in new onset diabetes seems a possible approach for T1D treatment.

Keywords: CXCL10; CXCR3; Cytokines; Type 1 diabetes; Viral infections.

PubMed Disclaimer

MeSH terms