We assume that the regression of this inflammation is the result of immune regulation, which is characterized by the change of interaction mode of dendritic cells. Firstly, we established a mouse model of airway disease driven by Th2 cells. When we exposed this mouse to OVA antigen for 8 weeks, all the inflammation disappeared.
Re-immunization and stimulation show immune response disorder to Th2 deviation, which is characterized by lack of airway eosinophils, IgE and Th2 cytokines. In addition to specific immune tolerance, other protective effects can be seen. Compared with acute airway inflammation, CD4+CD25+Foxp3+? T regulatory cells? PD- 1 and? IL- 10？ Protein expression decreased.
In addition, ICOS and? The inhibition of CD28 and the maturation of dendritic cells were also inhibited. Surprisingly, the inhibition process of this disease has long-term memory and cannot be caused by endotoxin signal pathway of TLR-4. In short, our results show that continuous exposure to allergens can eliminate Th2 cell-mediated airway inflammation, which is due to immune tolerance. This immune tolerance is antigen-dependent and expanded by other antigens. Moreover, this immune tolerance is characterized by the change of interaction between dendritic cells and T cells, which can last for a long time. Our data further speculate that the inhibitory mechanism of allergic airway diseases is different from the anti-inflammatory mechanism seen in acute eosinophilic airway inflammation. ?
Keywords: asthma; Airway inflammation; * * * stimulation; Mouse model; Immune tolerance?
Clinical relevance?
It is now clear that immune tolerance disorder leads to allergic airway inflammation. Our data show that it can be reconstructed despite exposure to immune tolerance. In addition, our research shows the characteristics of related immune mechanisms.