Protective and non-protective immunity in STIs.

It is certainly remarkable that the causative agents of sexually transmitted infections (STIs) induce long-lasting protective immune responses only occasionally and insufficiently ( T. pallidum, human papilloma viruses, herpes simplex virus, S. scabie) or not at all ( C. trachomatis, N. gonorrhoeae”, C. albicans, human immunodeficiency virus, T. vaginalis).

The reasons for this phenomenon are often microbe-related, but may also be due to peculiarities of the mucosal immune system. Evidence exists, for instance, that density and function of epithelial dendritic cells in the mucosa are different from those in the epidermis and, perhaps as a consequence of this, mucosal sensitization more often results in T cell non-responsiveness or anergy than epicutaneous sensitization.

The relatively poor functionality of the adaptive immune response in the defence against the various STI-causing microorganisms can sometimes by compensated by cells and molecules of the innate immune system. Good examples of this are the overexpression of certain anti-microbial peptides in the vaginal epithelium and the imiquimod-induced cytotoxic response of plasmacytoid dendritic cells against HPV-infected targets.

At a time where we are challenged with increased anti-microbial resistance to anti-microbial chemotherapy, research efforts are needed to better understand the mechanisms of microbe - host cell interactions and to use this knowledge for the development of better therapeutic strategies.