Mechanisms of allergic inflammation

Genetik yatkınlık ve çevreden gelen uyarılar T hücrelerinin, diğer inflamatuvar hücrelerin ve vücut dokularında bulunan hücrelerin yaşam sürelerini ve efektör fonksiyonlarını düzenlerler. T hücrelerindeki apoptoz ve periferal tolerans bozuklukları farklı alerjik fenotiplerini belirler. Yüksek IFN-g yapan aktive olmuş alerjen spesifik T hücreleri dolaşımda erken apoptoza gittikleri için atopik hastalıklarda immun yanıtı Th2 hücreleri yönüne çevirirler. Etkilenen dokularda bu hücreler efektör sitokinleri devreye sokarak epitel hücrelerinin aktivasyonunu ve apoptozunu da tetiklerler. Diğer taraftan monoallerjik nonatopik bireylerde T regulatuvar 1 hücreleri yerine alerjen spesifik Th2 hücreleri yönüne kaymış olan denge T hücre yanıtını belirler.

Allerjik inflamasyonun mekanizmaları

Genetic predisposition and environmental instructions tune thresholds for activation, effector functions and life span of T cells, other inflammatory cells and resident tissue cells. Defects in apoptosis and peripheral tolerance in T cells define different allergic phenotypes. High IFN-g-producing activated allergen-specific T cells predominantly undergo apoptosis in the circulation, skewing the immune response to surviving Th2 cells in atopic diseases. In affected tissues, these cells switch on effector cytokines, induce activation and apoptosis of epithelial cells. On the other hand, in monoallergic non-atopic individuals disturbed balance toward allergen-specific T helper 2 cells instead of T regulatory 1 cells characterize the T cell response.

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