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Protection against ...
Protection against type 1 diabetes upon Coxsackievirus B4 infection and iNKT-cell stimulation: role of suppressive macrophages
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Ghazarian, LN (författare)
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Diana, J (författare)
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Beaudoin, L (författare)
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- Larsson, PG (författare)
- Karolinska Institutet
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Puri, RK (författare)
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van Rooijen, N (författare)
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- Flodstrom-Tullberg, M (författare)
- Karolinska Institutet
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Lehuen, A (författare)
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(creator_code:org_t)
- 2013-10-18
- 2013
- Engelska.
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Ingår i: Diabetes. - : American Diabetes Association. - 1939-327X .- 0012-1797. ; 62:11, s. 3785-3796
- Relaterad länk:
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https://diabetes.dia...
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http://kipublication...
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https://doi.org/10.2...
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Abstract
Ämnesord
Stäng
- Invariant natural killer T (iNKT) cells belong to the innate immune system and exercise a dual role as potent regulators of autoimmunity and participate in responses against different pathogens. They have been shown to prevent type 1 diabetes development and to promote antiviral responses. Many studies in the implication of environmental factors on the etiology of type 1 diabetes have suggested a link between enteroviral infections and the development of this disease. This study of the pancreatropic enterovirus Coxsackievirus B4 (CVB4) shows that although infection accelerated type 1 diabetes development in a subset of proinsulin 2–deficient NOD mice, the activation of iNKT cells by a specific agonist, α-galactosylceramide, at the time of infection inhibited the disease. Diabetes development was associated with the infiltration of pancreatic islets by inflammatory macrophages, producing high levels of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α and activation of anti-islet T cells. On the contrary, macrophages infiltrating the islets after CVB4 infection and iNKT-cell stimulation expressed a number of suppressive enzymes, among which indoleamine 2,3-dioxygenase was sufficient to inhibit anti-islet T-cell response and to prevent diabetes. This study highlights the critical interaction between virus and the immune system in the acceleration or prevention of type 1 diabetes.
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