[Immunoglobulins E and inflammatory cells].

Immunoglobulins E (IgE) have a privileged relationship with inflammatory cells due to the fact that there are different receptors for their Fc fragment expressed on the cell's surface. Currently one recognises at least three types of receptor: high affinity receptors (Fc epsilon RI) which are present on the surface of mast cells, basophils, and Langerhans cells. The receptors of low affinity (Fc epsilon RII) are represented on the surface of numerous inflammatory cells (eosinophils, lymphocytes, platelets...) and some lectine type (epsilon BP) receptors which are present on polymorpho-nuclear neutrophils and activated macrophages. The IgE interaction in the presence of specific antigens on the receptor may lead to cellular activation by transduction mechanism which are becoming better understood. This sequence of events, combined with the mechanisms of immediate hypersensitivity lead to the liberation of mediators and cytokines which nature varies according to the cell type and its environment. Polymorpho-nuclear eosinophils, mast cells, basophils and many other cells comply with this type of activation. However, the relationship between IgE and cells is not limited to this type of activation response. In the absence of specific antigen, IgE may sometimes play an inhibitory role on cellular functions; it is the case of blood platelets and polymorpho-nuclear neutrophils. Finally, IgE also participates in normal mechanisms of immune defence and may perhaps, by their presence on the surface of the dentritic cells, be determining factors in the function of antigen presentation. The diversity of IgE action at cellular level may equally be observed at the level of the bronchus, on organ which is implicated in allergic pathology. Passive sensitisation of the human bronchus by IgE may have at least two types of effect on the contractile response observed in vivo: in the presence of specific antigen it enables the contraction of bronchial smooth muscles and in the absence of antigen it could change the contractile response to non-specific agonists as it is observed in vivo in bronchial hyper-reactivity.