Autor: |
Alyanakian, Marie-Alexandra, Gouarin, Christine, Chatenoud, Lucienne, Bach, Jean-François, Grela, Françoise, Aumeunier, Aude, Bardel, Emilie, Thieblemont, Nathalie, Chiavaroli, Carlo, Normier, Gérard |
Předmět: |
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Zdroj: |
Diabetes; Jan2006, Vol. 55 Issue 1, p179-185, 7p, 1 Chart, 6 Graphs |
Abstrakt: |
The onset of type 1 diabetes in NOD mice is delayed by oral administration of a bacterial extract (OM-85) and can be completely prevented by its intraperitoneal administration. Optimal prevention is observed when starting treatment at 3 or 6 weeks of age, and some effect is still observed with treatment at 10 weeks of age. Using genetically deficient mice and cytokine-neutralizing monoclonal antibodies, we demonstrate here that the therapeutic effect does not involve T-helper type 2 cytokines (interleukin [IL]-4 and -10) but is tightly dependent on transforming growth factor (TGF)-β. Natural killer T-cells also participate in the therapeutic effect because CD1d-/- NOD mice are partially resistant to the protective effect of OM-85. The question remains of the specificity of the protective effect of OM-85, which may include proinflammatory components. It will thus be important to further characterize the molecular components that afford protection from type 1 diabetes. Lipopolysaccharide is excluded, but other Toll-like receptor (TLR) agonists could be involved because OM-85 stimulated dendritic ceils and induced TGF-β production by splenocytes in a TLR-2-, TLR-4-, and MyD88-dependent fashion. [ABSTRACT FROM AUTHOR] |
Databáze: |
Complementary Index |
Externí odkaz: |
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