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<p>Chronic rhinosinusitis (CRS) is characterized by local inflammation of the upper airways and sinuses, persisting for at least 12&#xa0;weeks. The two forms of CRS include CRS with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP), and their immunological manifestations are distinct. Although less evidence is available regarding Non-Type 2 inflammation, it is established that Type 2 inflammation predominates in Western populations. While CRSwNP is historically linked to Type 2 inflammation, recent studies confirm significant endotypic heterogeneity, encompassing Type 1, Type 3, and mixed inflammatory patterns. Eosinophilia in CRSwNP nasal polyps (NPs) is a hallmark of the disease in Western nations. Inflammation in eosinophilic NPs is regulated by the Type 2 cytokine family members, especially interleukin-5 (IL-5) and interleukin-13 (IL-13). IL-5 strongly induces eosinophils, and IL-13 causes tissue remodeling, IgE-mediated responses, and an influx of eosinophils and T-helper Type 2 cells via activating macrophages, B cells, and epithelial cells. The production of Type 2 cytokines by these cells in eosinophilic NPs may be directly or indirectly influenced by cytokines originating from epithelial cells, such as thymic stromal lymphopoietin (TSLP), interleukin-33, and interleukin-1. Clinical studies revealed that monoclonal antibodies targeting IL-5, IL-4Ra, IgE, and TSLP are viable therapy options for CRSwNP patients.</p>

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Targeting Type-2 inflammation in chronic rhinosinusitis with nasal polyps: mechanisms, eosinophilia, and emerging therapies

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月22日

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  • Sahar Khorasani,
  • Mohammad Hasan Yousefi,
  • Somayeh Safarirad,
  • Hamed Afkhami,
  • Azin Khodadadi

摘要

Chronic rhinosinusitis (CRS) is characterized by local inflammation of the upper airways and sinuses, persisting for at least 12 weeks. The two forms of CRS include CRS with nasal polyps (CRSwNP) and CRS without nasal polyps (CRSsNP), and their immunological manifestations are distinct. Although less evidence is available regarding Non-Type 2 inflammation, it is established that Type 2 inflammation predominates in Western populations. While CRSwNP is historically linked to Type 2 inflammation, recent studies confirm significant endotypic heterogeneity, encompassing Type 1, Type 3, and mixed inflammatory patterns. Eosinophilia in CRSwNP nasal polyps (NPs) is a hallmark of the disease in Western nations. Inflammation in eosinophilic NPs is regulated by the Type 2 cytokine family members, especially interleukin-5 (IL-5) and interleukin-13 (IL-13). IL-5 strongly induces eosinophils, and IL-13 causes tissue remodeling, IgE-mediated responses, and an influx of eosinophils and T-helper Type 2 cells via activating macrophages, B cells, and epithelial cells. The production of Type 2 cytokines by these cells in eosinophilic NPs may be directly or indirectly influenced by cytokines originating from epithelial cells, such as thymic stromal lymphopoietin (TSLP), interleukin-33, and interleukin-1. Clinical studies revealed that monoclonal antibodies targeting IL-5, IL-4Ra, IgE, and TSLP are viable therapy options for CRSwNP patients.