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<p><i>Mycoplasma pneumoniae</i> pneumonia (MPP) is a highly prevalent form of community-acquired pneumonia (CAP) that can be complicated by severe extrapulmonary manifestations, leading to poor prognosis. The immunopathogenesis of MPP remains incompletely elucidated. This review synthesizes recent advancements, identifying host immune dysfunction and microbial immune evasion as the pivotal dual drivers of MPP immunopathogenesis. We detail how dysregulation of both innate and adaptive immunity—including impaired macrophage function, neutrophil-driven hyperinflammation, paradoxical natural killer (NK) cell activity, and imbalances in T-cell subsets—leads to ineffective pathogen clearance and promotes tissue damage. Concurrently, <i>Mycoplasma pneumoniae</i> perpetuates infection through strategies such as antigenic variation, the expression of an immunoglobulin-binding protein of <i>Mycoplasma</i> (IbpM), and intracellular invasion. Furthermore, we explore the role of autoimmune mechanisms, including molecular mimicry, in mediating extrapulmonary complications. Finally, we highlight the importance of translating these mechanistic insights into targeted immunotherapies and rational vaccine design, which are essential for overcoming current therapeutic limitations and improving clinical outcomes for patients with MPP.</p>

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Host immune dysfunction and Mycoplasma pneumoniae immune evasion: dual drivers of pathogenesis in Mycoplasma pneumoniae pneumonia

  • 期刊论文

  • 发表日期：

    2026年3月3日

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  • Hanxue Xiang,
  • Caopei Zheng,
  • Yu Wang,
  • Yuqing Sun,
  • Chengxia Li,
  • Miaotian Cai,
  • Yulin Zhang

摘要

Mycoplasma pneumoniae pneumonia (MPP) is a highly prevalent form of community-acquired pneumonia (CAP) that can be complicated by severe extrapulmonary manifestations, leading to poor prognosis. The immunopathogenesis of MPP remains incompletely elucidated. This review synthesizes recent advancements, identifying host immune dysfunction and microbial immune evasion as the pivotal dual drivers of MPP immunopathogenesis. We detail how dysregulation of both innate and adaptive immunity—including impaired macrophage function, neutrophil-driven hyperinflammation, paradoxical natural killer (NK) cell activity, and imbalances in T-cell subsets—leads to ineffective pathogen clearance and promotes tissue damage. Concurrently, Mycoplasma pneumoniae perpetuates infection through strategies such as antigenic variation, the expression of an immunoglobulin-binding protein of Mycoplasma (IbpM), and intracellular invasion. Furthermore, we explore the role of autoimmune mechanisms, including molecular mimicry, in mediating extrapulmonary complications. Finally, we highlight the importance of translating these mechanistic insights into targeted immunotherapies and rational vaccine design, which are essential for overcoming current therapeutic limitations and improving clinical outcomes for patients with MPP.