Target of acquired immunity in trichomoniasis vaginalis

Targets of Acquired Immunity in trichomoniasis vaginalis. The presence of parasite-specific immunoglobulin G and immunoglobulin A responses also indicates priming of helper Trichomoniasis cells, although the relevant antigens are largely unknown, as are the exact effects of antibodies on the parasites. One obvious target of protective antibody could be the ahesin molecules used by the parasite to facilitate close contact to host cells, a process previously shown to lead to efficient host cell destruction.

The molecular basis of adhesion of Trichomoniasis vaginalis has been investigated, and four antigenic surface molecules have also been implicated in the adhesion of Trichomoniasis vaginalis to vaginal epithelial cells; their expression is being upregulated during attachment to host cells.

Antibodies to these molecules protected target cells from parasite-mediated cytotoxicity, suggesting that antiadhesion immune responses could be important in in vivo protection against the pathogenic effects of Trichomoniasis vaginalis. However, our current understanding of immunity to Trichomoniasis vaginalis remains unsatisfactory, and it is not clear whether acquired immune responses are required for protection and, if so, what role is played by acquired immunity in containing or eliminating infections.

Although there is some evidence that protection may be achieved by immunization of laboratory animals, strong protective immunity does not seem to follow natural infection in humans. A recent study of patients infected with Trichomoniasis vaginalis and HIV indicated no evidence of increased levels or longevity of parasite infection in these patients compared to those in patients infected with Trichomoniasis vaginalis but not HIV.

These observations may indicate that innate immunity involving chemotaxis and subsequent influx of neutrophils is much more important than acquired immunity in controlling infections with Trichomoniasis vaginalis, since neutrophils are often the most numerous leukocytes present in response to infection .