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Lakartidningen · 2025

[Pan-neurofascin autoimmune nodopathy - an emerging and treatable differential diagnosis to Guillain-Barré syndrome].

СтатьяКлинический случайАннотация на английскомНазвание и аннотация: Перевод пока не подготовлен
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Kmezic Ivan, Eriksson Anders, Sundman Eva, Press Rayomand

Аннотация

BACKGROUND: Antigen-induced upregulation of cytokines, especially Th2-type cytokines, has been proven to be closely related to allergic inflammation in nasal allergy. CD4-positive T cells are supposed to play an important role not only in the induction of allergy but also in allergic inflammation.

METHODS: The anti-CD4 mAb was administered to the murine model of nasal allergy either at the beginning of sensitization, just before antigen challenge or during a topical booster sensitization. Then, the effects on the antigen-induced nasal responses and the serum level of antigen-specific IgE antibody were evaluated.

RESULTS: When the mAb was applied at the beginning of sensitization, the early-phase nasal symptoms and the late-phase nasal eosinophilia were significantly inhibited, and the 8-day passive cutaneous anaphylaxis (PCA) titer tended to be inhibited. When the mAb was applied just before the challenge, there were no differences in the nasal symptoms, the nasal eosinophilia or the 8-day PCA titer between the mAb-treated animals and the control animals. When the mAb was applied during a topical booster sensitization, the nasal eosinophilia, the 8-day PCA titer and histamine hypersensitivity were significantly suppressed in the treated animals.

CONCLUSION: CD4-positive T cells play an important role in the induction of IgE-mediated nasal allergy, occurrence of late-phase allergic inflammation and histamine hypersensitivity, but not in antigen-induced early-phase nasal symptoms in the murine model. In cases of chronic topical antigen exposure, however, the suppressive effects of a single application of the anti-CD4 mAb are not remarkable.

Предметные рубрики MeSH

ИП Урсолов Владлен Сергеевич

ИНН 500118482352 · ОГРНИП 314500117700049

Реквизиты и контакты