Protective Role of Infections and Vaccinations on Autoimmune Diseases

Bach, Jean‐François

doi:10.1006/jaut.2000.0478

Cited by 81 publications

(54 citation statements)

References 61 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…12,13 As activators of cytokine production in response to infection, TLRs may participate in early life Th1 immunophenotype development. 14,15 Genetic variation in these receptors may thus influence risk for either Th1 (infectious) or Th2 (atopic) disease. Additionally, two missense mutations of the TLR4 gene (Asp299Gly and Thr399Ile) have been associated with a decreased response to inhaled endotoxin in humans.…”

Section: Resultsmentioning

confidence: 99%

Toll-like receptor 6 gene (TLR6): single-nucleotide polymorphism frequencies and preliminary association with the diagnosis of asthma

et al. 2004

View full text Add to dashboard Cite

Toll-like receptor 6 (TLR6) is one of a series of highly conserved innate immune receptors. We resequenced TLR6 in DNA samples from 24 African Americans, 23 European Americans, and 24 Hispanic Americans, identifying 53 SNPs, 22 with an allele frequency 45%. Significant differences in SNP frequencies among the three populations were noted. In all, 11 SNPs caused amino-acid changes, including one with a frequency 45% in all three populations. Utilizing this SNP (Ser249Pro), we performed exploratory nested case-control disease-association studies, including one involving 56 African Americans with asthma and 93 African American controls. The minor allele of this SNP was associated with decreased risk for asthma (odds ratio 0.38, 95% CI 0.16-0.87, P ¼ 0.01), an effect consistent with the known biology of the toll-like receptors. Although replication of this finding in other, larger samples is needed, variation in TLR6 may have relevance to the pathogenesis of immunologically mediated diseases.

show abstract

Section: Resultsmentioning

confidence: 99%

Toll-like receptor 6 gene (TLR6): single-nucleotide polymorphism frequencies and preliminary association with the diagnosis of asthma

et al. 2004

View full text Add to dashboard Cite

show abstract

“…Collectively, the extended poliovirus hypothesis and the results presented here may be viewed as an extension of the hygiene hypothesis, which states that hosts who are less exposed to infectious agents are at higher risk for developing autoimmune disorders and allergies [37,38]. Indeed, it may not be the lack of enterovirus infections in the primary host that is detrimental, but rather the lack of maternal infectious exposure that is a contributing factor for disease development in offspring.…”

Section: Discussionmentioning

confidence: 99%

Previous maternal infection protects offspring from enterovirus infection and prevents experimental diabetes development in mice

et al. 2013

View full text Add to dashboard Cite

Aims/hypothesis Enterovirus (e.g. Coxsackie B virus serotypes [CVBs]) infections may be associated with development of type 1 diabetes. Studies conducted in several European countries have, however, shown an inverse correlation between the incidence of type 1 diabetes and the prevalence of enterovirus infections. These findings could in part be explained by an extension of the poliovirus hypothesis, suggesting that the absence of maternally transferred antibodies protecting offspring from early infection increases the risk for diabetes development. Experimental evidence supporting this hypothesis in type 1 diabetes is, however, lacking. As maternally transferred protection from infection is a crucial component of the extended poliovirus hypothesis, we here tested the hypothesis that previously infected females transfer protection against infection and diabetes to offspring.Methods The induction of CVB-specific maternal antibodies and transfer of protection from virus infection, replication and development of virus-induced diabetes to offspring was assessed using NOD and Socs1-transgenic NOD mice. Results Infected mice produced neutralising antibodies to CVB. Offspring from infected females were positive for neutralising antibodies and were strongly protected from both infection and experimental diabetes. Conclusions/interpretation Our study shows that maternally transferred antibodies protect offspring from enterovirus infection and virus-induced diabetes. This suggests that the absence of maternally provided protection increases the risk for severe outcomes after an enterovirus infection in offspring. Moreover, our findings may have implications for the design of prospective studies aimed at investigating the possible role of enterovirus infections in the aetiology of human type 1 diabetes.

show abstract

“…In contrast, several studies have shown that chronic infection can attenuate some peripheral and central pathological processes: complete Freund's adjuvant prevents the onset of experimental allergic encephalomyelitis (Bach, 2001), schistosomiasis can protect against asthma (Yang et al, 2007), coxsackievirus B3 can inhibit cardiomyopathy (Huber et al, 2006) and various infections can attenuate murine models of multiple sclerosis (Sewell et al, 2002). In some conditions, a pre-existing inflammation can induce brain neurodegeneration.…”

Section: Discussionmentioning

confidence: 99%

Decreased infarct size after focal cerebral ischemia in mice chronically infected with Toxoplasma gondii

et al. 2007

View full text Add to dashboard Cite

Abstract-To determine whether Toxoplasma gondii infection could modify biological phenomena associated with brain ischemia, we investigated the effect of permanent middle cerebral artery occlusion (MCAO) on neuronal survival, inflammation and redox state in chronically infected mice. Infected animals showed a 40% to 50% decrease of infarct size compared with non-infected littermates 1, 4 and 14 days after MCAO. The resistance of infected mice may be associated with increased basal levels of anti-inflammatory cytokines and/or a marked reduction of the MCAO-related brain induction of two pro-inflammatory cytokines, tumor necrosis factor-alpha and interferon-gamma (IFN␥). In addition, potential anti-inflammatory/neuroprotective factors such as nerve growth factor, suppressor of cytokine signaling-3, superoxide dismutase activity, uncoupling protein-2 and glutathione (GSH) were upregulated in the brain of infected mice. Consistent with a role of GSH in central cytokine regulation, GSH depletion by diethyl maleate inhibited Toxoplasma gondii lesion resistance by increasing the proinflammatory cytokine IFN␥ brain levels. Overall, these findings indicate that chronic toxoplasmosis decisively influences both the inflammatory molecular events and outcome of cerebral ischemia.

show abstract

Protective Role of Infections and Vaccinations on Autoimmune Diseases

Cited by 81 publications

References 61 publications

Toll-like receptor 6 gene (TLR6): single-nucleotide polymorphism frequencies and preliminary association with the diagnosis of asthma

Toll-like receptor 6 gene (TLR6): single-nucleotide polymorphism frequencies and preliminary association with the diagnosis of asthma

Previous maternal infection protects offspring from enterovirus infection and prevents experimental diabetes development in mice

Decreased infarct size after focal cerebral ischemia in mice chronically infected with Toxoplasma gondii

Contact Info

Product

Resources

About