NLRP3炎症小体对病毒感染提供多重防御，但是否促进特异性B细胞应答尚需证据。我们研究发现：HBV感染导致NLRP3炎症小体活化；慢性HBV感染选择性下调NLRP3炎症小体组分的转录；抑制炎症小体活性可下调初次B细胞应答。提示：NLRP3炎症小体可能促进HBV特异性B细胞免疫应答。为证明此假说，本项目拟用HDI HBV caspase-1-/-,NLRP3-/-,IL-1RI-/-小鼠模型，分析抗体初次应答不同时相点不同表型GCB频率，高频突变和抗体类型转换，以及HBV特异性抗体的动力学改变，探讨NLRP3炎症小体对GCB分化成熟的调控效应。本项目将促进对HBV免疫防御机制的理解，为建立HBV免疫治疗新策略提供思路。

NLRP3 inflammasome provide some protective role against viral infection. However, whether it shapes HBV-specific humoral immunity remain unknown. In previous research, we verified a high level of systemic NLRP3 inflammasome activation existed in chronic HBV infection. And HBV downregulates the transcription of NLRP3 inflammasome components selectively. In the HBV model of tree shrews, the inhibition of activity of NLRP3 inflammasome results in reduced primary antibody response. All the results mentioned above suggest NLRP3 inflammasome could support a protective role during the HBV infection through instigation of HBV-specific humoral immunity. In this project, we will investigate how NLRP3 inflammasome regulate the differentiation and maturation of GCB in the HBV hydrodynamic transfection model based on caspase-1-/-,NLRP3-/- and IL-1RI-/- mice through assay of the frequency of the GCB and plasma cell in different time points, somatic hypermutation and classic swtich recombination. This project will contribute to a comprehensive understanding of the establishment of the HBV defensive response; provide the novel strategy for HBV immunotherapy.