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<p>While immune dysregulation is implicated in sarcopenia, the causal roles of specific innate immune cell subsets and their functional states remain unclear. We conducted a two-sample Mendelian randomization (MR) analysis to assess the causal effects of 731 immune traits on core sarcopenia phenotypes. After false discovery rate correction, 14 robust associations were identified, revealing a state-dependent duality within myeloid cells. Specifically, a higher absolute count of pro-inflammatory CD14-CD16+ monocytes was linked to reduced right hand grip strength (RHGS), whereas a higher count of intermediate CD14+ CD16+ monocytes and increased CD16 expression on this subset were associated with improved strength. Conversely, the relative abundance of classical CD14+CD16- monocytes was positively associated with appendicular lean mass (ALM). Similarly, the relative abundance of total myeloid dendritic cells (DCs) correlated positively with lean mass, while a higher absolute count of activated CD62L-CD86+ DCs was linked to poorer strength. Reverse analysis largely supported the primary causal direction. These findings provide genetic evidence that specific innate immune subsets influence sarcopenia in a manner critically dependent on cellular identity and functional state, refining the mechanistic link between immunosenescence and muscle decline.</p>

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The causal effects of immune factors on sarcopenia-related phenotypes

  • 期刊论文

  • 发表日期：

    2026年8月4日

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  • Jin-Li Hou,
  • Yang Chai,
  • Jia-Xin Wu,
  • Ben Niu,
  • Fei-Yan Deng,
  • Shu-Feng Lei

摘要

While immune dysregulation is implicated in sarcopenia, the causal roles of specific innate immune cell subsets and their functional states remain unclear. We conducted a two-sample Mendelian randomization (MR) analysis to assess the causal effects of 731 immune traits on core sarcopenia phenotypes. After false discovery rate correction, 14 robust associations were identified, revealing a state-dependent duality within myeloid cells. Specifically, a higher absolute count of pro-inflammatory CD14-CD16+ monocytes was linked to reduced right hand grip strength (RHGS), whereas a higher count of intermediate CD14+ CD16+ monocytes and increased CD16 expression on this subset were associated with improved strength. Conversely, the relative abundance of classical CD14+CD16- monocytes was positively associated with appendicular lean mass (ALM). Similarly, the relative abundance of total myeloid dendritic cells (DCs) correlated positively with lean mass, while a higher absolute count of activated CD62L-CD86+ DCs was linked to poorer strength. Reverse analysis largely supported the primary causal direction. These findings provide genetic evidence that specific innate immune subsets influence sarcopenia in a manner critically dependent on cellular identity and functional state, refining the mechanistic link between immunosenescence and muscle decline.