The nasopharyngeal tonsil, or adenoid, is a major inductive site for the synthesis of J-chain-positive B cells that may migrate to other areas of the upper respiratory tract, such as the nasal mucosa, the parotid gland, the lacrimal gland, and the middle ear during inflammation. The production of secretory IgA by both the nasopharyngeal tonsil and the nasal mucosa plays a major role in local immune protection against bacteria and viruses. The release of cytokines from Th1 and Th2 lymphocytes must be appropriate for B cells to produce IgA. The factors or mechanisms responsible for this are not, at present, known, but it appears that there is a difference in the profiles of cytokine secretion by Th1 and Th2 lymphocytes in the adenoids in both otitis-prone, as well as nonotitis-prone children. We have suggested that if this specific immune system does not protect the host from invasion by potential pathogens, there are other modalities of therapy to protect the nasopharynx from colonization with pathogenic bacteria or viruses. These include the production of specific antibodies against bacterial surface proteins that have been identified as mucin-binding proteins. Alteration of the microbial flora with commensal organisms such as viridans streptococci can be utilized. These alpha-hemolytic streptococci probably function by producing an acid environment that prevents colonization of organisms such as nontypeable H. influenzae. Finally, the induction of specific SIgA by conserved outer membrane protein antigens of potential pathogens may be another strategy in the prevention of colonization of potential bacterial pathogens in the nasopharynx.