We have been studying developmental adaptations of T. cruzi to the vertebrate host, and in particular, surface membrane changes occurring during the morphogenesis of epimastigotes (vector stage) to metacyclic trypomastigotes (infective stage). A. Stage specific antigens recognized by monoclonal antibodies. A series of stage specific monoclonal antibodies were generated against metacyclic trypomastigotes. These antibodies were characterized as recognizing surface antigens with relative Mrs of 90 and 75k. The 90k species was found to be partially released into the medium upon culture of the parasites. B. Mechanism of ACP regulation by T. cruzi. As previously described by us, metacyclic trypomastigotes which normally evade lysis by the alternative complement pathway (ACP) can be made sensitive by prior treatment with pronase. We have now shown that this treatment effects ACP activation by facilitating the binding of Factor B to parasite bound C3b, a process which is inefficient in the non-enzyme exposed parasites. In addition, we have shown that the enzyme treatment selectively removes a 90k-115k glycoprotein (recognized by one of the monoclonals mentioned above) from the metacyclic surface, suggesting that this parasite molecule might be responsible for the regulation of ACP activation. Finally, a decay accelerating factor-like activity was detected in the supernatant of cultured metacyclic forms which also could account for the evasion of complement lysis by these vertebrate-adapted parasites.
