Beta cells are responsible for CXCR3-mediated T-cell infiltration in insulitis

Nat Med. 2002 Dec;8(12):1414-20. doi: 10.1038/nm1202-792. Epub 2002 Nov 4.


T cell-mediated loss of insulin-secreting beta cells in the islets of Langerhans is the hallmark of type 1 diabetes. The molecular basis for the directed migration of autoreactive T cells leading to insulitis is presently unknown. Here we demonstrate that in response to inflammation, beta cells secrete the chemokines CXC ligand 10 and CXC ligand 9, which specifically attract T-effector cells via the CXC chemokine receptor 3. In mice deficient for this receptor, the onset of type 1 diabetes is substantially delayed. Thus, in the absence of known etiological agents, CXC receptor 3 represents a novel target for therapeutic interference early in type 1 diabetes.

MeSH terms

  • Animals
  • Cells, Cultured
  • Chemokine CXCL10
  • Chemokines, CXC / physiology
  • Diabetes Mellitus, Type 1 / etiology
  • Inflammation / etiology
  • Inflammation / pathology
  • Islets of Langerhans / immunology*
  • Islets of Langerhans / pathology*
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Receptors, CXCR3
  • Receptors, Chemokine / physiology*
  • T-Lymphocytes / physiology*


  • Chemokine CXCL10
  • Chemokines, CXC
  • Cxcr3 protein, mouse
  • Receptors, CXCR3
  • Receptors, Chemokine