4.4 Article

Characterization of the anti- ? -Gal antibody profile in association with Guillain-Barr ? e syndrome, implications for tick-related allergic reactions

期刊

TICKS AND TICK-BORNE DISEASES
卷 12, 期 3, 页码 -

出版社

ELSEVIER GMBH
DOI: 10.1016/j.ttbdis.2021.101651

关键词

Tick; Alpha-Gal; Allergy; Immunology; Antibody; Alpha-Gal syndrome

资金

  1. Consejeria de Educacion, Cultura y Deportes, JCCM, Spain [CCM17-PIC-036 (SBPLY/17/180501/000185)]
  2. University of Castilla La Mancha (UCLM, Spain)
  3. Fondo Europeo de Desarrollo Regional, FEDER, EU
  4. Ministerio de Ciencia, Innovacion y Universidades, Spain [FJC-2018-038277I]
  5. UCLM

向作者/读者索取更多资源

Humans evolved by losing the ability to synthesize a certain sugar molecule, which led to the development of a protective response against pathogens with a specific protein modification, but also resulted in a newly diagnosed allergic disease related to mammalian meat consumption. Research found that patients with neurological disorders had significantly decreased antibody levels to the sugar molecule, while patients with tick-associated allergies did not show significant differences.
Humans evolved by losing the capacity to synthesize the glycan Gal?1-3Gal?1-(3)4GlcNAc-R (?-Gal), which resulted in the capacity to develop a protective response mediated by anti-?-Gal IgM/IgG antibodies against pathogens containing this modification on membrane proteins. As an evolutionary trade-off, humans can develop the alpha-Gal syndrome (AGS), a recently diagnosed disease mainly associated with allergic reactions to mammalian meat consumption. The etiology of the AGS is the exposure to tick bites and the IgE antibody response against ?-Gal-containing glycoproteins and glycolipids. The objective of this study was to characterize the anti-?-Gal antibody response in association with the immune-mediated peripheral neuropathy, Guillain-Barre? syndrome (GBS), and compare it with different factors known to modulate the antibody response to ?-Gal such as exposure to tick bites and development of allergic reactions in response to tick bites. The results showed a significant decrease in the IgM/IgG response to ?-Gal in GBS patients when compared to healthy individuals. In contrast, the IgM/IgG levels to ?-Gal did not change in patients with allergic reactions to tick bites. The IgE response was not affected in GBS patients, but as expected, the IgE levels significantly increased in individuals exposed to tick bites and patients with tick-associated allergies. These results suggest that the immune pathways of anti-?-Gal IgM/IgG and IgE production are independent. Further studies should consider the susceptibility to allergic reactions to tick bites in GBS patients.

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