Abstract
This primer focuses on a recently diagnosed tick-borne allergic disease known as the alpha-Gal syndrome (AGS). Tick bites induce in humans high levels of IgE antibodies against the carbohydrate Galα1-3Galβ1-(3)4GlcNAc-R (α-Gal) present on tick salivary glycoproteins and tissues of non-catarrhine mammals, leading to the AGS in some individuals. This immune response evolved as a conflict and cooperation between ticks and human hosts including their gut microbiota. The conflict is characterized by the AGS that mediate delayed anaphylaxis to red meat consumption and certain drugs such as cetuximab, and immediate anaphylaxis to tick bites. The cooperation is supported by the capacity of anti-α-Gal IgM and IgG antibody response to protect against pathogens with α-Gal on their surface. Despite the growing diagnosis of AGS in all world continents, many questions remain to be elucidated on the tick proteins and immune mechanisms triggering this syndrome, and the protective response against pathogen infection elicited by anti-α-Gal antibodies. The answer to these questions will provide information for the evaluation of risks, diagnosis and prevention of the AGS, and the possibility of using the carbohydrate α-Gal to develop vaccines for the control of major infectious diseases.
Highlights
This primer focuses on a recently diagnosed tick-borne allergic disease known as the alpha-Gal syndrome (AGS)
Most of the patients that become allergic, had tolerated red meat for many years before being sensitized by tick bites [10]. This finding suggests that while IgG and IgM antibody responses to α-Gal produced by some bacteria of the gut microbiota are beneficial as they protect against infection by pathogens such de la Fuente et al Parasites Vectors (2019) 12:154 as malaria parasites and tuberculosis mycobacteria, antiα-Gal IgE antibodies induced by tick bites break the oral tolerance to food allergens and induce anaphylactic reactions to tick α-Gal-containing salivary proteins [7,8,9,10,11,12,13,14,15]
The AGS has been associated with tick bites and constitutes a growingly diagnosed disease worldwide
Summary
This primer focuses on a recently diagnosed tick-borne allergic disease known as the alpha-Gal syndrome (AGS). Despite the growing diagnosis of AGS in all world continents, many questions remain to be elucidated on the tick proteins and immune mechanisms triggering this syndrome, and the protective response against pathogen infection elicited by anti-α-Gal antibodies. The answer to these questions will provide information for the evaluation of risks, diagnosis and prevention of the AGS, and the possibility of using the carbohydrate α-Gal to develop vaccines for the control of major infectious diseases. Apart from proteins with immunomodulatory activity, ticks produce non-protein molecules such as prostaglandin E2 (PGE2), which is synthesized in the tick salivary glands and secreted via the saliva into the feeding lesion [26, 28]
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