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<p>Innate lymphoid cells (ILCs) are critical regulators of early immune responses at mucosal barriers. As sentinels of the innate immune system, they rapidly detect infection-induced signals and initiate tissue-protective programs prior to the full activation of adaptive immunity. Emerging evidence shows that bacteria activate ILCs through multiple mechanisms, including direct recognition via pattern recognition receptors (PRRs), cytokine-mediated interactions with myeloid and epithelial cells, and metabolic and transcriptional modulation. Once activated, distinct ILC subsets coordinate antibacterial defense through cytotoxic activity and cytokine-driven regulation of macrophages, neutrophils, and epithelial cells. Notably, these pathways can be subverted by both pathogenic and commensal bacteria to manipulate ILC responses, enabling immune evasion and persistence, yet how bacterial signals are integrated and dynamically regulated by ILCs across tissues and disease contexts remains incompletely understood. Here, we synthesize recent progress in elucidating the molecular and cellular mechanisms underlying bacteria–ILC crosstalk, highlight emerging concepts and unresolved questions, and discuss how context-dependent ILC responses contribute to either host protection or disease progression. By integrating findings across infection models and mucosal environments, we propose a unifying framework for ILC-mediated antibacterial immunity and its dysregulation and highlight the therapeutic potential of targeting ILC-associated pathways as promising strategies for chronic and persistent bacterial infections.</p>

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The Dual Roles of Innate Lymphoid Cells in Antibacterial Defense and Bacterial Immune Evasion

  • 期刊论文

  • 发表日期：

    2026年7月10日

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  • Yuting Hu,
  • Huaqing Liu,
  • Qi Liu,
  • Pengfei Sun,
  • Changjiang Chen,
  • Zhou Sha,
  • Zhizeng Wang,
  • Haibo Wu

摘要

Innate lymphoid cells (ILCs) are critical regulators of early immune responses at mucosal barriers. As sentinels of the innate immune system, they rapidly detect infection-induced signals and initiate tissue-protective programs prior to the full activation of adaptive immunity. Emerging evidence shows that bacteria activate ILCs through multiple mechanisms, including direct recognition via pattern recognition receptors (PRRs), cytokine-mediated interactions with myeloid and epithelial cells, and metabolic and transcriptional modulation. Once activated, distinct ILC subsets coordinate antibacterial defense through cytotoxic activity and cytokine-driven regulation of macrophages, neutrophils, and epithelial cells. Notably, these pathways can be subverted by both pathogenic and commensal bacteria to manipulate ILC responses, enabling immune evasion and persistence, yet how bacterial signals are integrated and dynamically regulated by ILCs across tissues and disease contexts remains incompletely understood. Here, we synthesize recent progress in elucidating the molecular and cellular mechanisms underlying bacteria–ILC crosstalk, highlight emerging concepts and unresolved questions, and discuss how context-dependent ILC responses contribute to either host protection or disease progression. By integrating findings across infection models and mucosal environments, we propose a unifying framework for ILC-mediated antibacterial immunity and its dysregulation and highlight the therapeutic potential of targeting ILC-associated pathways as promising strategies for chronic and persistent bacterial infections.