细胞衰老会释放大量细胞因子、蛋白酶和生长因子，统称衰老相关分泌现象(SASP)。持续的SASP有助于衰老相关慢性炎症的形成，并与许多年龄相关性疾病有关。本文研究了免疫调节细胞因子B淋巴细胞活化因子(BAFF, 由TNFSF13B基因编码)在多个衰老模型中的表达和功能。首先，我们表征了BAFF在不同的衰老模型中的产生，包括老化的人类成纤维细胞(WI-38，IMR-90)和单核细胞白血病细胞(THP-1)，以及诱导老化的小鼠组织。然后我们发现，IRF1(干扰素调节因子1)是促进衰老中TNFSF13B mRNA转录的转录因子。我们发现抑制BAFF的产生会减轻成纤维细胞和单核细胞的衰老表型，减少IL6的分泌和SA-β-Gal染色。然而，BAFF对衰老程序的影响是细胞类型特异性的：在单核细胞中，BAFF促进NF-κB的早期活化和一般的SASP分泌，而在成纤维细胞中，BAFF有助于TP53(p53)的产生和功能。我们提出，BAFF在各种衰老模型中均上升，是一种可以用于老化治疗的潜在靶点。

Senescent cells release a variety of cytokines, proteases, and growth factors collectively known as the senescence-associated secretory phenotype (SASP). Sustained SASP contributes to a pattern of chronic inflammation associated with aging and implicated in many age-related diseases. Here, we investigated the expression and function of the immunomodulatory cytokine BAFF (B-cell activating factor; encoded by the TNFSF13B gene), a SASP protein, in multiple senescence models. We first characterized BAFF production across different senescence paradigms, including senescent human diploid fibroblasts (WI-38, IMR-90) and monocytic leukemia cells (THP-1), and tissues of mice induced to undergo senescence. We then identified IRF1 (interferon regulatory factor 1) as a transcription factor required for promoting TNFSF13B mRNA transcription in senescence. We discovered that suppressing BAFF production decreased the senescent phenotype of both fibroblasts and monocyte-like cells, reducing IL6 secretion and SA-β-Gal staining. Importantly, however, the influence of BAFF on the senescence program was cell type-specific: in monocytes, BAFF promoted the early activation of NF-κB and general SASP secretion, while in fibroblasts, BAFF contributed to the production and function of TP53 (p53). We propose that BAFF is elevated across senescence models and is a potential target for senotherapy.