时间标签：数据日期 2026-11-05 · 生成时间 2026-11-05 05:30（Asia/Shanghai）｜ 检索窗口 PubMed edat 2026/11/02 – 2026/11/06 ｜ 情报发生日期 2026-11-05
研究问题
When coupling mechanisms become imbalanced, whether through enhanced resorption or impaired formation, net bone loss ensues, representing the common pathological basis of metabolic bone diseases such as osteoporosis (4).Osteocytes are the most abundant and longest-lived cells in bone tissue.
方法
To integrate these multi-level interactions, we first present a conceptual framework illustrating how senescent immune cells collectively disrupt bone remodeling homeostasis (Figure 1).Figure 1Immunosenescence-driven bone remodeling imbalance.；First, whereas previous reviews generally treat immune aging as a systemic background factor, we focus specifically on the bone marrow microenvironment as the shared niche in which immune senescence and skeletal aging proceed as an interconnected process.；Second, we highlight genuinely emerging evidence, including bone marrow-specific immune senescence revealed by single-cell and spatial omics (Section 3.6) and direct causal evidence linking senescent immune subsets to skeletal phenotypes, rather than restating well-established associations.
核心结论
The origin of this field can be traced to the discovery that activated T cells express RANKL and directly regulate osteoclast generation: in 1999, Kong et al. demonstrated that activated T lymphocytes participate in bone loss and joint destruction in adjuvant arthritis by expressing the OPG ligand (i.e., RANKL), establishing adaptive immune cells for the first time as direct drivers of osteoclastogenesis (23).；Over the subsequent two decades, research has demonstrated that immune cells not only promote bone resorption by secreting RANKL and inflammatory factors, but also inhibit osteoclast generation through interferon-γ (IFN-γ), interleukin (IL)-10, and TGF-β, and additionally influence bone formation by modulating osteoblast and osteocyte function (25, 26).The deepening of osteoimmunology research has brought about an important shift in the understanding of age-related bone loss.；To integrate these multi-level interactions, we first present a conceptual framework illustrating how senescent immune cells collectively disrupt bone remodeling homeostasis (Figure 1).Figure 1Immunosenescence-driven bone remodeling imbalance.
局限
However, data on bone metabolic outcomes from immune interventions in elderly populations remain limited, with most bone metabolism evidence coming from indirect observations (43).；In addition, changes in NET formation tendency of aged neutrophils are associated with bone metabolic diseases; the dual role of NET components as autoantigens and pro-osteoclastic signals warrants further investigation (98).；Upstream strategies targeting Th17 differentiation and blocking IL-17A itself have been validated as effective in inflammatory bone diseases, and their value in senile osteoporosis warrants exploration (113, 118).6.3TregsTregs inhibit osteoclast generation and maintain bone homeostasis through multiple mechanisms.
对本项目的价值
中高价值：属「衰老细胞清除 / SASP 轴」方向；细胞衰老 / senolytics / SASP栏目可用作本项目文献库与综述素材。 ｜ 价值分 3.1/5（★★★☆☆）
全文来源
PubMed PMC JATS（正文 118,839 字符，题名指纹 1.0，已过 PubMed PMCID 官方关联 + 题名指纹 + 正文长度归属校验）
原文题录
- 中文题名：免疫衰老与骨重塑：从免疫细胞衰老到骨髓微环境驱动的骨骼老化
- 英文标题：Immunosenescence and bone remodeling: from immune cell senescence to skeletal aging through the bone marrow microenvironment.
- 期刊与标识：Frontiers in immunology · PMID 42979376 · DOI 10.3389/fimmu.2026.1979955 · PMC PMC13729129