Tick salivary proteins metalloprotease and allergen-like p23 are associated with response to glycan α-Gal and mycobacterium infection
Abstract 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 d...
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| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Nature Portfolio
2025-03-01
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| Series: | Scientific Reports |
| Subjects: | |
| Online Access: | https://doi.org/10.1038/s41598-025-93031-3 |
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| Summary: | Abstract 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. |
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| ISSN: | 2045-2322 |