Inflammation is a natural defence mechanism of the body to protect against pathogens. It is induced by immune cells, such as macrophages and neutrophils, which are rapidly recruited to the site of infection, mediating host defence. The processes for eliminating inflammatory cells after pathogen clearance are critical in preventing sustained inflammation, which can instigate diverse pathologies. During chronic inflammation, the excessive and uncontrollable activity of the immune system can cause extensive tissue damage. New therapies aimed at preventing this over-activity of the immune system could have major clinical benefits. Here, we investigated the role of the pro-survival Bcl-2 family member A1 in the survival of inflammatory cells under normal and inflammatory conditions using murine models of lung and peritoneal inflammation. Despite the robust upregulation of A1 protein levels in wild-type cells upon induction of inflammation, the survival of inflammatory cells was not impacted in A1-deficient mice compared to wild-type controls. These findings indicate that A1 does not play a major role in immune cell homoeostasis during inflammation and therefore does not constitute an attractive therapeutic target for such morbidities.

炎症是身体抵御病原体的天然防御机制。它由免疫细胞（如巨噬细胞和嗜中性粒细胞）诱导，这些细胞迅速募集到感染部位，介导宿主防御。病原体清除后消除炎症细胞的过程对于防止持续炎症至关重要，而持续炎症会引发多种病理。在慢性炎症期间，免疫系统过度和无法控制的活动会导致广泛的组织损伤。旨在防止免疫系统过度活跃的新疗法可能具有重要的临床益处。在这里，我们使用肺和腹膜炎症小鼠模型研究了促生存 Bcl-2 家族成员 A1 在正常和炎症条件下炎症细胞存活中的作用。与野生型对照相比，A1缺陷小鼠。这些发现表明 A1 在炎症期间的免疫细胞稳态中不发挥主要作用，因此不构成此类发病率的有吸引力的治疗靶点。