Allergic Alveoli's: The Lung's Immune Paradox in Hypersensitive Pneumonitis (EAA/HP)

AuthorMohammad Shiravi Khouzanien
AuthorKrishnaveni Kandasamyen
OrcidMohammad Shiravi Khouzani [0000-0003-2150-7233]en
OrcidKrishnaveni Kandasamy [0009-0009-9000-1974]en
Issued Date2024-08-31en
AbstractAllergic alveolitis/hypersensitive pneumonitis (EAA/HP) in its acute phase and allergic asthma in the chronic phase can be triggered by pigeon allergies. These allergies induce an immune response marked by elevated immunoglobulin E (IgE) levels, which block FCER-1 receptors on mast cells. This blockage prevents the release of histamine, leukotrienes C4, and prostaglandin D4, responsible for smooth muscle contraction and vascular leakage. Additionally, IgE can block FceRI receptors on basophils, forming IgE-FC complexes and stimulating CD23 and HEK-293 cells, while also increasing lung alveolar inflammation. Combining Cε2 with omalizumab can lower free IgE levels and block FceRI and CD23.en
DOIhttps://doi.org/10.5812/ijp-137727en
KeywordAA/HPen
KeywordHEK-293 Cellen
KeywordPigeon Allergyen
KeywordTSLPen
KeywordOmalizumaben
PublisherBrieflandsen
TitleAllergic Alveoli's: The Lung's Immune Paradox in Hypersensitive Pneumonitis (EAA/HP)en
TypeReview Articleen

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