树突状细胞（DCs）是固有免疫和适应性免疫的桥梁，近年来发现DCs除了具有免疫原性，还具有免疫耐受性。耐受型DCs日益成为过敏性疾病、自身免疫疾病等领域的新热点。我们前期发现低剂量脂多糖和过敏原（OVA）活化可使骨髓来源的DCs形成耐受表型，将其过继给哮喘受鼠，可逆转过敏性气道炎症和气道高反应性。若将该DCs的SOCS3基因敲除再过继给受鼠则废除了其免疫抑制性。本项目拟深入研究该耐受型DCs表型，以及LPS触发的LPS-TLR4与SOCS3/Jak-STATs信号交互作用的分子机制。耐受型DCs所诱导的Treg亚群及其在致炎环境中的稳定性。明确是否SOCS3基因过表达也可通过影响DCs的表面分子、分泌和迁移功能使其具有耐受性等科学问题。本项目的完成，将创新性地初步揭示脂多糖活化的骨髓来源的树突状细胞（BMDCs）在过敏性哮喘中的免疫调节机制，为耐受型DCs早日进入临床应用提供科学依据。

Dendritic cells (DCs) are the bridge between innate immunity and adaptive immunity. DCs not only play an immunogenic role, but also have immune tolerance. Tolerogenic DCs have increasingly become a new hotspot in the field of allergic diseases, autoimmune diseases and so on. We previously found that low-dose lipopolysaccharide and allergen (OVA) pulsed bone marrow-derived DCs (BMDCs) can lead to tolerogenic DCs (DC lps). Adoptive transfer of DC lps to recipient mice reversed inflammatory cell infiltration and airway hyperreaction in asthmatic mice. However, SOCS3-/-DC lps adoptive transfer abolished the previous immunosuppression. Based on this findings, we would like to further explore LPS-activated tolerogenic DCs’ phenotype, the cell signal transduction system triggered by LPS, like LPS-TLR4 and SOCS3/Jak-STATs and their interaction, the specific subtypes of Treg induced by tolerogenic DCs and their stability in inflamed tissue. Whether SOCS3 gene overexpression in DCs can lead to immune tolerance via changing its surface marker, secretion and migration are also big issues. We are sure that this project will initially reveal the role and immunoregulatory mechanism of lipopolysaccharide-activated bone marrow-derived dendritic cells (BMDCs) in allergic asthma, and provide insights for the clinical application of tolerogenic DCs in the future.