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Siglecs as mediators of the pancreatic cellular crosstalk in diabetes

The mechanisms of the immune and endocrine cell interaction within the islet and resulting β-cell death are highly complex and largely unknown. To investigate the cellular crosstalk in the pancreas and how its disturbance leads to... ver más

31/12/2015

UBREMEN

1M€

Presupuesto del proyecto: 1M€

Líder del proyecto

UNIVERSITAET BREMEN No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Fecha límite participación Sin fecha límite de participación.

Financiación concedida El organismo FP7 notifico la concesión del proyecto el día 2015-12-31 No tenemos la información de la convocatoria

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UBREMEN

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Líder del proyecto

UNIVERSITAET BREMEN No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 1M€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto The mechanisms of the immune and endocrine cell interaction within the islet and resulting β-cell death are highly complex and largely unknown. To investigate the cellular crosstalk in the pancreas and how its disturbance leads to insufficient insulin production is important to understand the pathology of the disease. This is the major goal of this project. Activation of inflammation is not only a trigger for β-cell destruction, but also a major factor for the metabolic syndrome, including insulin resistance and complications of diabetes. Signalling and activation of immune cells is facilitated by secreted pro-inflammatory stimulators and via cell-cell interactions. I propose that a group of adhesion and signalling molecules, the Siglecs (sialic acid–binding immunoglobulin (Ig)-like lectins) mediate such interactions. They are responsible for immune system activation and have been initially found in cells of hematopoietic origin. I made the groundbreaking observation of cell type specific Siglec expression in the human pancreas: Siglecs were differentially expressed in glucagon producing α-cells, and in insulin producing β-cells. A diabetic milieu had an inductive effect on Siglec expression in the α-cells, but lead to decreased β-cell specific Siglecs. This loss of Siglecs in the β-cell could be detrimental and result in an excessive cytokine release and in turn switches on Siglec responses in neighbouring cells. In my proposed studies I will investigate the role of Siglecs in the cellular network in islets and in the circulation to probe whether changes in Siglec expression are causative in the development of diabetes. My project is a pioneer and multidisciplinary study combining the current knowledge of glycobiochemistry and β-cell biology in diabetes. The project uses multi-model cell systems of healthy and diseased human pancreatic tissue, isolated human islets, isolated human β-cells as well as diabetic mouse models, all of them being absolutely novel and high-risk to a large extend.

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