β cells are responsible for CXCR3-mediated T-cell infiltration in insulitis
S Frigerio, T Junt, B Lu, C Gerard, U Zumsteg… - Nature medicine, 2002 - nature.com
S Frigerio, T Junt, B Lu, C Gerard, U Zumsteg, GA Holländer, L Piali
Nature medicine, 2002•nature.comT cell–mediated loss of insulin-secreting β 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, β 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 …
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, β 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 …
Abstract
T cell–mediated loss of insulin-secreting β 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, β 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.
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