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<p>The alpha-Gal syndrome (AGS) evolved as a catastrophic selection associated with anti-α-Gal IgM/IgG protective response against pathogen infection and tick-borne food allergy caused by IgE-type antibodies against this glycan present in glycoproteins and glycolipids from mammalian meat and derived products. The immune response to α-Gal is modulated by tick salivary proteins with and without α-Gal modifications in combination with tick saliva non-protein fraction. Herein, we characterized the role of tick salivary proteins, metalloprotease and allergen-like p23 in AGS and protection against tuberculosis in the AGS zebrafish animal model. Metalloprotease and p23 are involved in allergic reactions after mammalian meat consumption through upregulation of pro-inflammatory protein-coding genes <i>prkdc</i>, <i>tlr2</i>, <i>tnfα</i> and <i>il1b</i>. Challenge with <i>Mycobacterium marinum</i> activated Th1-mediated immune protective response with reduced pathogen infection, ameliorating Th2-associated allergic reactions associated with AGS. These results highlight molecular mechanisms modulated by tick proteins in response to α-Gal and provide insights to reduce AGS impact on human health.</p>

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Tick salivary proteins metalloprotease and allergen-like p23 are associated with response to glycan α-Gal and mycobacterium infection

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年3月14日

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  • Rita Vaz-Rodrigues,
  • Lorena Mazuecos,
  • Marinela Contreras,
  • Almudena González-García,
  • Marta Rafael,
  • Margarita Villar,
  • José de la Fuente

摘要

The alpha-Gal syndrome (AGS) evolved as a catastrophic selection associated with anti-α-Gal IgM/IgG protective response against pathogen infection and tick-borne food allergy caused by IgE-type antibodies against this glycan present in glycoproteins and glycolipids from mammalian meat and derived products. The immune response to α-Gal is modulated by tick salivary proteins with and without α-Gal modifications in combination with tick saliva non-protein fraction. Herein, we characterized the role of tick salivary proteins, metalloprotease and allergen-like p23 in AGS and protection against tuberculosis in the AGS zebrafish animal model. Metalloprotease and p23 are involved in allergic reactions after mammalian meat consumption through upregulation of pro-inflammatory protein-coding genes prkdc, tlr2, tnfα and il1b. Challenge with Mycobacterium marinum activated Th1-mediated immune protective response with reduced pathogen infection, ameliorating Th2-associated allergic reactions associated with AGS. These results highlight molecular mechanisms modulated by tick proteins in response to α-Gal and provide insights to reduce AGS impact on human health.