The common mucosal immune system (CMIS) consists of an integrated cross-communication pathway of lymphoid tissues made up of inductive and effector sites for host protection against pathogenic microorganisms. Major effector molecules of the CMIS include
IgA antibodies and
cytokines,
chemokines and their corresponding receptors.
Secretory IgA (S-
IgA), the major
immunoglobulin, is induced by gut-associated lymphoreticular tissue (GALT)-derived B cells with the help of Th1- and Th2-type CD4(+) T lymphocytes. Cytotoxic T lymphocytes (CTLs) in the mucosal epithelium, a subpopulation of intraepithelial lymphocytes (IELs), also help maintain the mucosal barrier. The CMIS is unique in that it can provide both positive and negative signals for the induction and regulation of immune responses in both the mucosal and systemic compartments after oral or nasal
antigen exposure. Prevention of
infection through mucosal surfaces can be achieved by the CMIS through connections between inductive (e.g. GALT) and effector tissues. When
vaccine antigens are enterically administered together with mucosal adjuvants [e.g.
cholera toxin (CT), heat-labile toxin produced by Escherichia coli (LT) and
IL-12],
antigen-specific Th1/Th2 and
IgA B cell responses are induced simultaneously in the mucosal effector compartment. Since these
antigen-specific immune responses are not generated by oral
vaccine without mucosal adjuvant, safe and effective adjuvants for the induction of
antigen-specific S-
IgA and CTL responses are essential for the development of mucosal
vaccines for protection against
infectious diseases. Finally, recent findings suggest the presence of a CMIS-independent
IgA induction pathway, which also must be considered in the development of mucosal
vaccines.