The authors describe a case of an allergic affection in a patient with occupational exposure to latex allergens with a history of anaphylactic reaction to poppy seed and reaction to the antigens of apples, oranges, tangerines, peanuts and bananas, revealed by the method CAP Phadiatop. A marked reaction was initiated after the use of a shampoo containing volatile banana oil. The authors emphasize the high incidence of latex allergy, the manifestations of which may be encountered also in clinical ophthalmology.

• MeSH
• alergie na latex komplikace   diagnóza   MeSH
• anafylaxe etiologie   MeSH
• dospělí MeSH
• lidé MeSH
• nemoci z povolání diagnóza   MeSH
• potravinová alergie komplikace   diagnóza   MeSH
• Check Tag
• dospělí MeSH
• lidé MeSH
• mužské pohlaví MeSH
• Publikační typ
• anglický abstrakt MeSH
• časopisecké články MeSH
• kazuistiky MeSH
• práce podpořená grantem MeSH

The α-Gal syndrome (AGS) is a type of allergy characterized by an IgE antibody (Ab) response against the carbohydrate Galα1-3Galβ1-4GlcNAc-R (α-Gal), which is present in glycoproteins from tick saliva and tissues of non-catarrhine mammals. Recurrent tick bites induce high levels of anti-α-Gal IgE Abs that mediate delayed hypersensitivity to consumed red meat products in humans. This was the first evidence that tick glycoproteins play a major role in allergy development with the potential to cause fatal delayed anaphylaxis to α-Gal-containing foods and drugs and immediate anaphylaxis to tick bites. Initially, it was thought that the origin of tick-derived α-Gal was either residual blood meal mammalian glycoproteins containing α-Gal or tick gut bacteria producing this glycan. However, recently tick galactosyltransferases were shown to be involved in α-Gal synthesis with a role in tick and tick-borne pathogen life cycles. The tick-borne pathogen Anaplasma phagocytophilum increases the level of tick α-Gal, which potentially increases the risk of developing AGS after a bite by a pathogen-infected tick. Two mechanisms might explain the production of anti-α-Gal IgE Abs after tick bites. The first mechanism proposes that the α-Gal antigen on tick salivary proteins is presented to antigen-presenting cells and B-lymphocytes in the context of Th2 cell-mediated immunity induced by tick saliva. The second mechanism is based on the possibility that tick salivary prostaglandin E2 triggers Immunoglobulin class switching to anti-α-Gal IgE-producing B cells from preexisting mature B cells clones producing anti-α-Gal IgM and/or IgG. Importantly, blood group antigens influence the capacity of the immune system to produce anti-α-Gal Abs which in turn impacts individual susceptibility to AGS. The presence of blood type B reduces the capacity of the immune system to produce anti-α-Gal Abs, presumably due to tolerance to α-Gal, which is very similar in structure to blood group B antigen. Therefore, individuals with blood group B and reduced levels of anti-α-Gal Abs have lower risk to develop AGS. Specific immunity to tick α-Gal is linked to host immunity to tick bites. Basophil activation and release of histamine have been implicated in IgE-mediated acquired protective immunity to tick infestations and chronic itch. Basophil reactivity was also found to be higher in patients with AGS when compared to asymptomatic α-Gal sensitized individuals. In addition, host resistance to tick infestation is associated with resistance to tick-borne pathogen infection. Anti-α-Gal IgM and IgG Abs protect humans against vector-borne pathogens and blood group B individuals seem to be more susceptible to vector-borne diseases. The link between blood groups and anti-α-Gal immunity which in turn affects resistance to vector-borne pathogens and susceptibility to AGS, suggests a trade-off between susceptibility to AGS and protection to some infectious diseases. The understanding of the environmental and molecular drivers of the immune mechanisms involved in AGS is essential to developing tools for the diagnosis, control, and prevention of this growing health problem.

• Klíčová slova
• IgE, food allergy, red meat allergy, ticks, α-Gal syndrome (AGS),
• MeSH
• alergeny imunologie   MeSH
• anafylaxe etiologie   MeSH
• červené maso MeSH
• genetická predispozice k nemoci MeSH
• hmyzí proteiny imunologie   MeSH
• imunoglobulin E metabolismus   MeSH
• interakce genů a prostředí MeSH
• klíšťata MeSH
• kousnutí klíštětem komplikace   imunologie   MeSH
• lidé MeSH
• potravinová alergie komplikace   etiologie   imunologie   MeSH
• tvorba protilátek MeSH
• zkřížené reakce MeSH
• zvířata MeSH
• Check Tag
• lidé MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• přehledy MeSH
• Názvy látek
• alergeny MeSH
• hmyzí proteiny MeSH
• imunoglobulin E MeSH

Foreign proteins penetrate across the wall of rabbit jejunum takes place within the first eight hours after birth. Sensitization by foreign protein (cow's milk protein) during early postnatal ontogeny is the cause of death of artificially fed germfree rabbits at the age of 21-23 d.

• MeSH
• anafylaxe etiologie   MeSH
• gnotobiologické modely MeSH
• intestinální absorpce MeSH
• jejunum metabolismus   MeSH
• králíci metabolismus   MeSH
• mléčné bílkoviny škodlivé účinky   imunologie   metabolismus   MeSH
• novorozená zvířata metabolismus   MeSH
• potravinová alergie etiologie   MeSH
• skot MeSH
• zvířata MeSH
• Check Tag
• králíci metabolismus   MeSH
• skot MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• Názvy látek
• mléčné bílkoviny MeSH