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CD49D IN DIABETES

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Role of the alpha4 integrin CD49d in Type 1 Diabetes mellitus prevention and t...

Role of the alpha4 integrin CD49d in Type 1 Diabetes mellitus prevention and treatment Type-1 Diabetes mellitus (T1D) is caused by destruction of insulin-producing tissues by autoreactive T lymphocytes, which leads to insulin deficiency. The high frequency of T1D, as well as the significant T1D-associated morbidity... ver más

02/09/2011

GUF

100K€

Presupuesto del proyecto: 100K€

Líder del proyecto

JOHANN WOLFGANG GOETHEUNIVERSITAET FRANKFURT... 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 2011-09-02 No tenemos la información de la convocatoria

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1 Participantes

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Líder del proyecto

JOHANN WOLFGANG GOETHEUNIVERSITAET FRANKFURT... No se ha especificado una descripción o un objeto social para esta compañía.

TRL 4-5

Presupuesto del proyecto 100K€

Fecha límite de participación Sin fecha límite de participación.

Descripción del proyecto Type-1 Diabetes mellitus (T1D) is caused by destruction of insulin-producing tissues by autoreactive T lymphocytes, which leads to insulin deficiency. The high frequency of T1D, as well as the significant T1D-associated morbidity and the substantial burden from long-term sequelae despite state-of-the-art insulin substitution therapies underscore the urgency of developing causal treatments. Protection of remaining islet cell mass at T1D diagnosis and (potentially) subsequent islet cell regeneration could palliate or cure T1D and reduce long-term morbidity and mortality. The alpha-4 integrin is a dominant homing receptor for inflammatory lymphocytes, and blockade of alpha-4 adhesion is therapeutic in a variety of inflammatory conditions, including autoimmune diseases, in mice and humans. Thus continued substitution of anti-functional alpha-4 antibodies from birth could prevent T1D in the spontaneously diabetic NOD mouse. Such an approach is, however, not clinically applicable to patients, since the risk of T1D can not be predicted at birth. Therefore, we here propose to test the hypothesis that by ablation of alpha-4 integrin adhesion during pre-diabetes (normoglycemic insulitis) or during early diabetes (recent onset of hyperglycemia), the continued recruitment of autoreactive T-cells to inflamed pancreatic tissue might be arrested. It is proposed that this might protect the remaining insulin producing cells, and thus, depending on the regenerative capacity of the pancreatic islets, might prevent or delay T1D if initiated during pre-diabetes (secondary prevention) or cure or palliate T1D if initiated early after its onset (tertiary prevention). This hypothesis will be tested in a new genetic mouse model of inducible ablation of alpha-4 integrin in the NOD strain. Since human alpha-4 adhesion blocking drugs are already available, these studies are testing a modality with immediate potential as a treatment for newly diagnosed patients with T1D.

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