FP7Реинтеграция2008–2011

HASKODIABETES · Adenosine receptors in diabetes

7РП — „Хора“ (Действия „Мария Кюри“)

Период
2008-04-01 → 2011-03-31
Финансиране от ЕС
75 000 €
Участници
1
Схема
MC-IRG

Линиите свързват координатора с партньорите.

Накратко на български

Аденозиновите рецептори и техният ефект върху баланса на имунните клетки се изследват при диабет тип 1. Това помага да се разбере как тези рецептори могат да намалят възпалението и да предпазят клетките на панкреаса от имунна атака.

Този кратък обзор е генериран от изкуствен интелект

Кратко обяснение, генерирано от езиков модел по текста на CORDIS. Оригиналът е по-долу.

Резултати накратко

Adenosine receptors in diabetes

Several autoimmune diseases are characterised by common alterations in the Th1 versus Th2 and IL-12/TNF-a versus IL-10 balance. In rheumatoid arthritis (RA), multiple sclerosis (MS), type 1 diabetes mellitus, autoimmune thyroid disease (ATD) and Crohn's disease, the balance is skewed toward Th1 activity and an excess of IL-12 and TNF-a production, whereas Th2 activity and the production of IL-10 are deficient. Type 1 diabetes or insulin-dependent diabetes mellitus (IDDM) result from an organ-specific immune-mediated attack on pancreatic ß-cells. Dr. Haskó and his colleagues have shown (Haskó et al. J. Immunol. 164: 1013-1019, 2000) that adenosine receptor occupancy with inosine significantly increased IL-4 production and decreased IFN-gamma production in the pancreas; this finding indicates a shift of cytokines towards a Th2 bias. Since adenosine is a potent endogenous autocrine anti-inflammatory and immunosuppressive molecule that is released from cells into the extracellular space at sites of inflammation and tissue injury, and protective effects of adenosine receptor stimulation have been observed in various models of autoimmune disease, such as rheumatoid arthritis, multiple sclerosis, colitis, and hepatitis (see Haskó and Cronstein, Trends in Immunol. 25: 33-39, 2004), investigations of whether the subtypes of adenosine receptors that are involved in mediating the Th1/Th2 balance also regulate autoimmune diabetes are promising. Dr. Haskó and his group have shown the following: - Activation of the adenosine A2A receptor protects peripherial CD4+ T-lymphocytes from activation-induced cell death. -

Текст от CORDIS, на английски · Данни: CORDIS, © Европейски съюз

Цел на проекта

Adenosine receptors are expressed on immune cells and other tissues thought to regulate inflammatory events in mammals. Adenosine receptors, when activated by endogenous ligands or exogenous analogs, may repress inflammatory and immune pathways that lead to the destruction of pancreatic islets in models of type I diabetes and islet graft rejection. Building on our observations that inosine and NECA, two adenosine receptor agonists, inhibit diabetes and islet graft rejection in non-obese diabetic mice and multiple-low-dose-streptozotocin-treated mice, we postulate that certain adenosine receptor subtypes play a protective role in these type 1 diabetic mouse models. There are four types of adenosine receptors, all of which are members of the G protein-coupled family of receptors. The genes for these receptors have been analyzed in detail and they are designated A1, A2A, A2B, and A3. In this proposal we will attempt to delineate the exact roles for the various adenosine receptors in modulating the development of diabetes. By identifying which receptor(s) mediate the adenosine-mediated suppression of diabetes, we can utilize this information to develop new therapeutic approaches that specifically target the receptor(s) of interest.

Оригинален текст от CORDIS (на английски).

Участници

  • HUN-REN KISERLETI ORVOSTUDOMANYI KUTATOINTEZET · BUDAPESTКоординаторУнгария

Връзки

Данни: CORDIS, © Европейски съюз