Review article: Local and systemic regulation of mucosal immunity

An increased interest in mucosal immunity has stemmed from the identification of novel T-cell populations and developments in oral vaccines and oral tolerance. The development of physiological inflammation is antigen driven. Upon recognition of antigen, the lamina propria (LP) is populated with lymphocytes and activated peripheral cells acquire the capacity to home to the gut. Antigen entry to the gut is via follicle-associated epithelium or M cells. The antigen now interacts with macrophages or CD4+ cells, and go on to the Peyer's patch where B cells undergo a transforming growth factor beta (TGF-beta)-mediated isotope switch to immunoglobulin (Ig) A. TGF-beta may also play a role in the development of oral tolerance. The intestinal epithelium is seen as the site for the activation of CD8+ suppressor cells. Controlled inflammation is therefore explained by the interaction of LP lymphocytes and intra-epithelial cells (IEC). IECs are capable of extending processes that express regulatory surface molecules coupled with antigen processed from luminal uptake. CD8+ T-cell activation is favoured over CD4+ T-cell activation due to the size of the antigenic binding peptide. The result is suppressed inflammation. Other antigen-presenting cells (APCs) and dendritic cells may also contribute to local immunosuppression.