Expression of B7 co-stimulatory molecules and CD1a antigen by alveolar macrophages in allergic bronchial asthma

Lung allergen recognition that takes place in the airways of asthmatic subjects is still a controversial matter.

We hypothesized that a rapid allergen recognition process requires the presence, at the mucosal surface, of professional APC, such as B7+ alveolar macrophages (AM) and/or CD1+ dendritic cells, which usually have a lower expression in the normal human lung.

Studies were performed on bronchoalveolar lavage (BAL) fluid collected from 10 untreated allergic subjects and 10 adult normal volunteers. Further controls consisted of five untreated pulmonary sarcoidosis (PS) and four extrinsic allergic alveolitis (EAA) individuals. To ascertain whether T helper 2-type cytokines or allergen influence B7 and CD1 antigen expression, in vitro studies were carried out using unprimed (naive) cord blood plastic-adherent monocytes.

Cytofluorymetric analysis revealed that AM from asthmatics, unlike those from normal subjects or patients with PS or EAA, overexpressed B7-2, CD1a and, to a lesser extent, B7-1 surface molecules. Immunohistochemical studies confirmed the presence of CD1+ dendritic cells in the BAL fluid from asthmatic subjects. On in vitro cultured naive cord blood monocytes both purified Dermatophagoides pteronyssinus allergen and T-cell cytokines, i.e. IL-4 and granulocyte macrophage colony-stimulating factor, induced surface expression of B7-2 and CD1a receptors, whereas they had no appreciable effect on that of B7-1 membrane molecule.

Taken together, these findings support the proposal that airways of atopic individuals are equipped with professional APC that synergize with allergen-specific T cells for the recognition of intact allergens. When the recognition process takes place, asthmatic symptoms could develop in genetically susceptible individuals.