On the Mechanisms of the Protective Effect of Infections on Type 1 Diabetes

Feillet, Hélène; Bach, Jean‐François

doi:10.1080/17402520400004557

Cited by 22 publications

(11 citation statements)

References 36 publications

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“…There is a clear parallel trend toward decreased infectious load in these countries linked to improved hygiene and medical care, including extensive usage of vaccinations and antibiotics (2)(3). A similar association is observed in animal models of the disease, such as nonobese diabetic (NOD) mice and Bio-Breeding (BB) rats.…”

mentioning

confidence: 63%

Transforming Growth Factor-β and Natural Killer T-Cells Are Involved in the Protective Effect of a Bacterial Extract on Type 1 Diabetes

et al. 2006

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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 (interleu- kin

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confidence: 63%

Transforming Growth Factor-β and Natural Killer T-Cells Are Involved in the Protective Effect of a Bacterial Extract on Type 1 Diabetes

et al. 2006

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“…These and other associations, sometimes discrepant (Borchers et al, 2010), are obviously the reflection of underlying molecular events. Most of these events are unknown but some has been extensively discussed in previous reviews (Cooke, 2009;Feillet & Bach, 2004;von Herrath, 2009). A variety of associations with viruses have been reported for human T1D, including rubella, mumps, and cytomegalovirus infections.…”

Section: Environmental Factors and T1d Incidencementioning

confidence: 99%

Echovirus Epidemics, Autoimmunity, and Type 1 Diabetes

Diaz-Horta¹,

Sarmiento²,

Baj³

et al. 2011

Type 1 Diabetes - Pathogenesis, Genetics and Immunotherapy

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“…Environmental exposure to TLR agonists has also been linked to protection from autoimmune disease in humans (18). Furthermore, mice lacking TLR4 and TLR9 are more susceptible to EAE induced by immunization with TLR agonists (19), and lupus-prone mice lacking TLR9 develop more severe spontaneous systemic lupus erythematosus (20).…”

mentioning

confidence: 99%

IL-10 Mediates Resistance to Adoptive Transfer Experimental Autoimmune Encephalomyelitis in MyD88−/− Mice

Cohen

Nussbaum³

2009

The Journal of Immunology

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MyD88 is an adaptor molecule that functions in the innate signaling induced by proinflammatory adjuvants that interact with TLRs. Mice lacking MyD88, for example, resist active experimental autoimmune encephalomyelitis (EAE) induced by immunization with an encephalitogenic myelin oligodendrocyte glycoprotein (MOG) peptide in CFA. We reasoned that MyD88−/− mice, nevertheless, should be susceptible to EAE mediated by adoptive transfer of activated encephalitogenic T cell lines, which do not require adjuvant signaling for their effector functions. We now report, however, that mice lacking MyD88 also resist adoptive EAE mediated by an anti-MOG T cell line that is strongly encephalitogenic in wild-type (WT) mice. The transferred anti-MOG T cells proliferated, secreted INF-γ, and migrated to the CNS in the MyD88−/− mice, as they did in WT mice, but inflammatory infiltrates did not progress and clinical EAE did not develop. The resistance of the MyD88−/− mice to adoptive EAE mediated by the otherwise encephalitogenic T cells was found to result from the secretion of IL-10 by recipient T cells of two different specificities: those specific for MOG and those responding to the T cell clone itself—both anticlonotypic and antiergotypic T regulators were detected. IL-10–producing anti-MOG T cells isolated from immunized MyD88−/− mice suppressed the induction of active EAE in WT recipients. Moreover, the absence of IL-10 production in MyD88/IL-10 double-knockout mice rendered the mice susceptible to adoptive transfer of EAE. Thus, MyD88 signaling appears to be a key factor in determining the cytokine phenotype of T cells involved in autoimmune inflammation and regulation.

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On the Mechanisms of the Protective Effect of Infections on Type 1 Diabetes

Cited by 22 publications

References 36 publications

Transforming Growth Factor-β and Natural Killer T-Cells Are Involved in the Protective Effect of a Bacterial Extract on Type 1 Diabetes

Transforming Growth Factor-β and Natural Killer T-Cells Are Involved in the Protective Effect of a Bacterial Extract on Type 1 Diabetes

Echovirus Epidemics, Autoimmunity, and Type 1 Diabetes

IL-10 Mediates Resistance to Adoptive Transfer Experimental Autoimmune Encephalomyelitis in MyD88−/− Mice

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