时间标签：数据日期 2026-10-31 · 生成时间 2026-11-01 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/10/28–2026/10/31 ｜ 情报发生日期 2026-10-31
研究问题
These studies found that in the absence of CD38 expression, immune cell infiltration was unaffected while AHR was decreased in naive mice as well as upon individual acute challenges with ovalbumin, Alterneria alternata, tumor necrosis factor alpha (TNF-α), or interleukin 13 (IL-13).；Given previous studies suggest that CD38 promotes pro-inflammatory responses and AHR in asthma, we hypothesized that Cd38 knockout mice administered chronic mixed allergen would have reduced AHR and immune cell infiltration compared to wild-type mice.
方法
Mouse studies were approved by the Institutional Animal Care and Use Committee (IACUC) at Abigail Wexner Research Institute at Nationwide Children’s Hospital.；Values are expressed at mean ± SEM, and P ≤ 0.05 was considered statistically significant.
核心结论
Reduced lung function is a key symptom of allergic airway inflammation.；There were no significant differences in AHR between PBS challenged Cd38+/+ and Cd38−/− mice ().；Upon challenge with 25 and 50 mg/mL methacholine, MA+GMP challenged Cd38−/− mice had significantly greater AHR compared to all treatment groups (). ‖ 结论：Our data suggest that CD38 may be important for type 1-associated immune responses that negatively regulate type 2 inflammation.
局限
These studies suggest that the lack of CD38 may lead to reduced IFN-γ production by NK cell populations, leading to expansion of ILC2 populations that release type 2 cytokines to enhance AHR.；Since CD38 is known to associate with the T cell receptor (TCR) and contribute to immune synapse activation, it will be important to more comprehensively evaluate how loss of CD38 affects Th1, Th2, and Th9 cell populations in future studies.；Future studies comparing the phenotypes of chronic allergen exposure in young versus aged Cd38−/− mice would aid in understanding the age dependency of CD38 in severe allergic airway inflammation.
对本项目的价值
★☆☆☆☆ 炎症衰老是几乎所有慢性老年病的公共通路，也是最有希望做「抗炎但保留免疫」解耦的靶点。
全文来源
PMC JATS 全文（正文 28,767 字符，已过标题/DOI 逐字归属校验）
原文题录
- 英文标题：Loss of CD38 promotes severe allergic airway inflammation and hyperresponsiveness in mice.
- 期刊与标识：Immunohorizons · PMID 42950088 · DOI 10.1093/immhor/vlag055
B 级证据分级：B 级（同行评议临床前研究，主要为动物模型）
本文核心结论来自动物模型或体外细胞学，属临床前证据，不能外推至人体。「延长健康寿命」「改善功能」等表述在小鼠中的意义，与人类临床结局之间仍有距离。
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