| Abstract: | Pollinosis is a model physio-pathology for IgE-dependent diseases. Rhinitis and conjunctivitis are the parent symptoms, with asthma a non-exceptional complication. The mechanisms are linked to an immuno-allergic inflammation; the observed differences are due to specific anatomo-physiologies of the sensitive cells. The pollen allergens are collected by the CPA and expressed after cleavage into peptides, at the surface of the CPA in association with class II HLA molecules. T-lymphocytes recognise the complex HLA-peptide molecules. Type Th2 lymphocytes produce the cytokines that the necessary for the synthesis of IgE (IL4, IL13...). At the stage of silent clinical sensitivity the precocious and delayed effector stages of immediate hypersensitivity follow. The precocious stage corresponds with degranulation of cells that express Fc epsilon R1, for release of vaso-active and lipid mediators that produce the immediate symptoms of pollinosis. The delayed phase corresponds with a flood of eosinophils, which release their toxic proteins proteins and also take part in oedema and nasal obstruction. Mucosal innervation, neurotransmitters and neuromediators also intervene in the modulation of symptoms. |
