Conversion of Trypanosoma cruzi Tc52 released factor to a protein inducing apoptosis

• Type: Article in International Scientific Journal
• Date: 2005

Authors

Borges, M (Author) Other; Cordeiro da Silva, A (Author) FFUP; Vergnes, B (Author) Other; Sereno, D (Author) Other; Ouaissi, A (Author) Other

Journal

Title: TISSUE & CELL

Vol. 37

Pages: 469-478

ISSN: 0040-8166

Publisher: CHURCHILL LIVINGSTONE

Indexing

ISI Web of Knowledge - 3 Citations

Scopus - 3 Citations

Scientific classification

FOS: Medical and Health sciences > Basic medicine

Other information

Authenticus ID: P-000-0DJ

DOI: 10.1016/j.tice.2005.09.001

Abstract (EN): In this study Tc52, a Trypanosoma cruzi released protein, which exerts an immunoregulatory activity, was converted to a molecular form with altered biological function. Indeed, the genetic fusion of Tc52 to a carrier protein, the Shistosoma japonicum glutathione S-transferase (Tc52-Sj26), was shown to induce apoptosis in spleen cells from BALB/c or CBA mice and the human T-cell leukemic cell line (CEM). Cell death by apoptosis was evidenced by the following criteria: (1) increased binding of Annexin V to rTc52-treated spleen cells; (2) the presence of an ordered cleavage of the DNA backbone; (3) double labeling showed increased number of T cells undergoing apoptosis upon incubation with rTc52; (4) the use of a CEM cell line and TUNEL assay allowed to show in situ DNA fragmentation. Surprisingly, intraperitoneal injections of rTc52 to BALB/c mice, which were then infected with T cruzi, resulted in increased parasiteamia levels and congruent to 2.5 times increase of macrophages number. Since native Tc52 could not trigger, apoptosis of T cells we could hypothesized that the fusion of Tc52 with Sj26 led to conformational changes resulting in apoptosis inducing properties of rTc52. The possible in vivo physiopathological implications of these finding were discussed.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 10