The mucosa of the upper respiratory tract is protected by a secretory immune system which is under complex immunoregulatory control. B cells with a potential for J-chain expression are initially stimulated in mucosa-associated lymphoid tissue (probably including the tonsils) and thereafter migrate through lymph and blood to glandular sites where they differentiate to immunoglobulin-producing immunocytes. Most locally produced immunoglobulin normally consists of dimeric IgA which is selectively transported through serous glandular cells by means of an epithelial receptor protein called the secretory component (SC). IgM is also subjected to SC-mediated transport. In patients with selective IgA deficiency, secretory IgA is lacking, but it may be satisfactorily replaced by protective secretory IgM. In other IgA-deficient patients, however, immunoregulatory compensation gives rise to a large number of IgD-producing cells in respiratory mucosae. IgD cannot act as a secretory antibody and these patients are prone to have recurrent infections. There are thus large individual variations in the secretory immune system, which in the future hopefully may be subjected to regulatory manipulation.