Immunoprofile of α‐Gal‐ and B‐antigen‐specific responses differentiates red meat‐allergic patients from healthy individuals

Apostolović, Danijela; Rodrigues, Rui Da Silva; Thomas, Pierre; Starkhammar, Maria; Hamsten, Carl; Hage, Marianne van

doi:10.1111/all.13400

Cited by 44 publications

(46 citation statements)

References 22 publications

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“…These differences could reflect the tick species, the community of microbiota living inside the ticks, or temporal changes in the tick saliva-derived factors throughout the duration of feeding, including protein changes in the saliva of lone star ticks as previously reported ( 102 – 105 ). Meat allergic patients show a Th2-skewed profile, as measured by higher α-gal IgE, IgG1 and IgG4 levels ( 106 ). This suggests that tick bites of affected individuals drive sensitization to α-gal by promoting Th2-mediated immune responses, possibly through induced antibody class switching by tick salivary PGE2, leading to an increase in the frequency of B cells producing α-gal-specific IgE ( 107 ).…”

Section: Ige Immune Responses In Allergymentioning

confidence: 99%

B Cell Responses in the Development of Mammalian Meat Allergy

2020

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Studies of meat allergic patients have shown that eating meat poses a serious acute health risk that can induce severe cutaneous, gastrointestinal, and respiratory reactions. Allergic reactions in affected individuals following meat consumption are mediated predominantly by IgE antibodies specific for galactose-α-1,3-galactose (α-gal), a blood group antigen of non-primate mammals and therefore present in dietary meat. α-gal is also found within certain tick species and tick bites are strongly linked to meat allergy. Thus, it is thought that exposure to tick bites promotes cutaneous sensitization to tick antigens such as α-gal, leading to the development of IgE-mediated meat allergy. The underlying immune mechanisms by which skin exposure to ticks leads to the production of α-gal-specific IgE are poorly understood and are key to identifying novel treatments for this disease. In this review, we summarize the evidence of cutaneous exposure to tick bites and the development of mammalian meat allergy. We then provide recent insights into the role of B cells in IgE production in human patients with mammalian meat allergy and in a novel mouse model of meat allergy. Finally, we discuss existing data more generally focused on tick-mediated immunomodulation, and highlight possible mechanisms for how cutaneous exposure to tick bites might affect B cell responses in the skin and gut that contribute to loss of oral tolerance.

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Section: Ige Immune Responses In Allergymentioning

confidence: 99%

B Cell Responses in the Development of Mammalian Meat Allergy

2020

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“…Although IgG4 is often considered part of a traditional type 2 immune response, high-titer IgG4 to a-gal has not consistently been reported in individuals with a-gal syndrome. 44,45,47 Interestingly, the effect of blood type on antiea-gal immunity and incidence of infectious diseases was lately reported by Cabezas-Cruz et al, 48 indicating that susceptibility to malaria and tuberculosis correlated positively with the frequency of blood type B in endemic regions. These diseases are caused by pathogens with a-gal on their surface.…”

Section: Interactions With B Antigenmentioning

confidence: 97%

“…43,44 This finding suggests that IgE response to a-gal may result from class switch of preexisting B cells. 41,45,46 However, several questions remain regarding the mechanisms of a-gal specific IgE production from the B-cell subsets in meat allergic individuals. Although IgG4 is often considered part of a traditional type 2 immune response, high-titer IgG4 to a-gal has not consistently been reported in individuals with a-gal syndrome.…”

Section: Interactions With B Antigenmentioning

confidence: 99%

Galactose α-1,3-galactose phenotypes

Levin

Apostolović

Biedermann

et al. 2019

Annals of Allergy, Asthma & Immunology

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Galactose a-1,3-galactose (a-gal) is a carbohydrate epitope found on proteins and lipids in nonprimate mammals and present in foods (particularly organ or fat-rich red meat) and medications (eg, cetuximab, certain vaccines, and antivenoms), where it causes delayed onset and immediate-onset anaphylaxis. Several species of ticks contain a-gal epitopes and possibly salivary adjuvants that modulate the immune response for IgE production and promote clinical reactivity to the epitope. Risk factors for a-gal syndrome include exposure to ticks of particular species, and age and sex differences possibly reflect the prevalence of these exposures in different cohorts and thus vary according to setting. Symptoms are skewed toward urticaria and a high prevalence of isolated abdominal reactions. The reason and mechanisms for delayed onset of food-related anaphylaxis are not clear but may involve the kinetics of allergen digestion and processing or immunologic presentation via a different mechanism from usual immediate type food allergy.

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“…To address the possibility that exposure to house cats could also be a relevant factor in a-Gal sensitization, as has been suggested by some reports, we investigated a cohort from an area where ticks are very rare. 28,29 Detailed information about cat exposure, as well as IgG to Felinus domesticus 1 as a marker of exposure, was available from a population-based study in Northern Sweden that we have previously investigated for asthma. 20 In this cold and arid region that straddles the Arctic Circle ticks are rare and there has been little report of mammalian meat allergy.…”

Section: Further Evidence For a Connection With Tick Bitesmentioning

confidence: 99%