Acute respiratory distress syndrome (ARDS) is an organ failure syndrome caused by overactivation of the immune system. Mesenchymal stem cells (MSCs) have been found to be effective in ARDS therapy due to their excellent immunomodulatory abilities; however, people are concerned about the safety of infusing exogenous cells. We found that rat lung-resident mesenchymal stem cells (LRMSCs) (Sca-1⁺CD45⁻CD31⁻) played important roles in regulating inflammation in the lungs during the pathogenesis of ARDS. LRMSCs could regulate the production of cytokines (TNF-α, MCP-1, and IL-10) by both innate and adaptive immune cells following LPS stimulation in vivo or in vitro. We also found that Herpes Virus Entry Mediator (HVEM) expression in LRMSCs enhanced the immunomodulatory ability of LRMSCs, and expression of the HVEM ligand B and T Lymphocyte Attenuator (BTLA) in innate and adaptive immune cells was required. The clarification of this immunoregulatory mechanism may provide evidence for ARDS therapy mediated by mobilizing endogenous MSCs in the future.

急性呼吸窘迫综合征（ARDS）是由免疫系统过度激活引起的器官衰竭综合征。间充质干细胞（MSC）由于其出色的免疫调节能力而在ARDS治疗中有效。但是，人们担心注入外源细胞的安全性。我们发现，大鼠肺居民间充质干细胞（LRMSCs）（SCA-1 ⁺ CD45 ^- CD31 ^-）在ARDS发病过程中在调节肺部炎症中起重要作用。在体内或体外LPS刺激后，LRMSCs可以通过先天和适应性免疫细胞调节细胞因子（TNF-α，MCP-1和IL-10）的产生。我们还发现，LRMSC中的疱疹病毒进入介体（HVEM）表达增强了LRMSC的免疫调节能力，并且需要先天性和适应性免疫细胞中HVEM配体B和T淋巴细胞衰减剂（BTLA）的表达。这种免疫调节机制的阐明可能为将来动员内源性MSC介导的ARDS治疗提供证据。