Treg stability in viral infection and autoimmunity

病毒感染和自身免疫中 Treg 的稳定性

基本信息

项目摘要

Our hypothesis is that viral infections have strong and diverging effects on different Treg populations. Our preliminary data indicate that Foxp3+ Tregs (adaptive or naturally occurring) and IL-10+ Tregs are affected by viral infections. The underlying mechanisms are proposed to be related to the modulation of APCs, in particular interferons and TLRs, resulting in strong effects on Treg activation, stability, which could be reflected in changes in the DNA methylation status ofthe Foxp3 promoter, and cytokine production, reflected in changes in the overall pattern of epigenetic markers in the genome. Clearly defining the underlying mechanisms and their precise effects will allow us not only to better understand the response of the immune system to viral infections, but to devise better strategies to induce Tregs for the treatment of chronic inflammatory disorders such as IBD, T1D and asthma. Aim 1: Do acute or chronic viral infections destabilize Foxp3 and/or IL-10 expression and Treg activity in vitro or in vivo? Using Foxp3 and IL-10 gene reporter mice, we will test our hypothesis that Foxp3 expression and IL-10 production are modulated during viral infection, and that this occurs differentially depending on whether the infection is acute (LCMV Armstrong) or chronic (LCMV Clone 13). We will compare effector functions of Tregs before, during, and after viral infections. Aim 2: How do Tregs influence the outcome of viral infections, autoimmunity, and asthma? Here we will test our hypothesis that different Treg types, in spite of their efficacy, are not comparable in terms of outcome and function in particular disease situations in vivo. Aim 3: How do viral infections affect Tregs stability and function mechanistically? Preliminary data indicate that Treg function is affected via APCs rather than a direct influence of viral infections on Tregs. In addition TLR2 appears to modulate and eventually expand and invigorate Foxp3+ Tregs. We propose that players in the innate immune system,such as DCs and TLRs, along with endogenous ligands, such as heat shock proteins (HSPs), play an important role in determining the outcome.
我们的假设是,病毒感染对不同的Treg群体有强烈而不同的影响。我们的

项目成果

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Matthias G. Von Herrath其他文献

Matthias G. Von Herrath的其他文献

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{{ truncateString('Matthias G. Von Herrath', 18)}}的其他基金

Treg stability in viral infection and autoimmunity
病毒感染和自身免疫中 Treg 的稳定性
  • 批准号:
    8495227
  • 财政年份:
    2013
  • 资助金额:
    $ 46.53万
  • 项目类别:
Specificity of CD8 cells in islets from type 1 diabetes patients
1 型糖尿病患者胰岛中 CD8 细胞的特异性
  • 批准号:
    8655830
  • 财政年份:
    2011
  • 资助金额:
    $ 46.53万
  • 项目类别:
Specificity of CD8 cells in islets from type 1 diabetes patients
1 型糖尿病患者胰岛中 CD8 细胞的特异性
  • 批准号:
    8261913
  • 财政年份:
    2011
  • 资助金额:
    $ 46.53万
  • 项目类别:
Specificity of CD8 cells in islets from type 1 diabetes patients
1 型糖尿病患者胰岛中 CD8 细胞的特异性
  • 批准号:
    8195256
  • 财政年份:
    2011
  • 资助金额:
    $ 46.53万
  • 项目类别:
Specificity, Phenotype and Function of Pancreatic CD8 T Cells in Human Type 1 Diabetes
人类 1 型糖尿病中胰腺 CD8 T 细胞的特异性、表型和功能
  • 批准号:
    9238399
  • 财政年份:
    2011
  • 资助金额:
    $ 46.53万
  • 项目类别:
Specificity of CD8 cells in islets from type 1 diabetes patients
1 型糖尿病患者胰岛中 CD8 细胞的特异性
  • 批准号:
    8451478
  • 财政年份:
    2011
  • 资助金额:
    $ 46.53万
  • 项目类别:
Specificity of CD8 cells in islets from type 1 diabetes patients
1 型糖尿病患者胰岛中 CD8 细胞的特异性
  • 批准号:
    8828063
  • 财政年份:
    2011
  • 资助金额:
    $ 46.53万
  • 项目类别:
Specificity, Phenotype and Function of Pancreatic CD8 T Cells in Human Type 1 Diabetes
人类 1 型糖尿病中胰腺 CD8 T 细胞的特异性、表型和功能
  • 批准号:
    10061526
  • 财政年份:
    2011
  • 资助金额:
    $ 46.53万
  • 项目类别:
Treg stability in viral infection and autoimmunity
病毒感染和自身免疫中 Treg 的稳定性
  • 批准号:
    8006796
  • 财政年份:
    2010
  • 资助金额:
    $ 46.53万
  • 项目类别:
How IL-10R blockade can resolve persistent viral infections
IL-10R 阻断如何解决持续性病毒感染
  • 批准号:
    7919813
  • 财政年份:
    2009
  • 资助金额:
    $ 46.53万
  • 项目类别:

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