Does native Trypanosoma cruzi calreticulin mediate growth inhibition of a mammary tumor during infection

摘要: For several decades now an antagonism between Trypanosoma cruzi infection and tumor development has been detected. The molecular basis of this phenomenon remained basically unknown until our proposal that T. Calreticulin (TcCRT), endoplasmic reticulum-resident chaperone, translocated-externalized by the parasite, may mediate at least important part effect. Thus, recombinant TcCRT (rTcCRT) in vivo antiangiogenic antitumor activities. However, relevant question whether effect is indeed mediated native chaperone (nTcCRT), remains open. Herein, using specific modified anti-rTcCRT antibodies (Abs), we have neutralized activity extracts thereof, thus identifying nTcCRT as a valid mediator Polyclonal F(ab’)2 Ab fragments were used to reverse capacity rTcCRT inhibit EAhy926 endothelial cell (EC) proliferation, detected BrdU uptake. Using these fragments, also challenged nTcCRT, during infection, growth aggressive mammary adenocarcinoma line (TA3-MTXR) mice. Moreover, determined Abs epimastigote extract (EE). Finally, effects treatments on histology evaluated. ECs proliferation was reversed defining them probes interfere with function. Consequently, experimental growth. EE, again protein anti conventional histological parameters, infected animals those treated less invasive tumors observed while, expected, treatment increased malignancy. We identified translocated/externalized responsible for infections cruzi.