Biochemical characterization of a factor produced by trypomastigotes of Trypanosoma cruzi that accelerates the decay of complement C3 convertases.

摘要: Infective- and vertebrate-stage trypomastigotes of Trypanosoma cruzi resist serum killing by the alternative complement pathway, whereas noninfective vector-stage epimastigotes, from which derive, are serum-sensitive. This form developmental preadaption is commonly observed in protozoan parasites, but its mechanisms poorly understood. We have demonstrated previously that spontaneously shed molecules interfere with formation accelerate intrinsic decay C3 convertases, a finding may explain evasion lysis trypomastigotes. now describe partial purification characterization T. convertase inhibitor supernatant culture metacyclic tissue Decay-accelerating activity for both classical pathway convertases copurifies on anion-exchange fast protein liquid chromatography chromatofocusing 35S-labeled 87-93 kDa, pI 5.6-5.8. The labeled components destroyed papain retained concanavalin A-Sepharose, procedures remove functional decay-accelerating supernatant. 87-93-kDa immunoprecipitated sera patients chronically infected cruzi, not antisera to any known regulatory proteins human cascade. Lytic chagasic associated antibody reactivity against inhibition activity. factor first developmentally regulated microbial be biochemically characterized.