This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Tambourgi, D V Articles by Ogden, G B Search for Related Content PubMed PubMed Citation Articles by Tambourgi, D V Articles by Ogden, G B

 Previous Article  |  Next Article 

Infect Immun. 1993 September; 61(9): 3656-3663

A partial cDNA clone of trypomastigote decay-accelerating factor (T-DAF), a developmentally regulated complement inhibitor of Trypanosoma cruzi, has genetic and functional similarities to the human complement inhibitor DAF.

Departamento de Imunologia, Universidade de São Paulo, Brazil.

ABSTRACT

Resistance to complement-mediated lysis in Trypanosoma cruzi is due to the expression of complement-regulatory factors by the virulent developmental forms of this protozoan parasite. An 87- to 93-kDa molecule, which we have termed T-DAF (trypomastigote decay-accelerating factor), is present on the surface of the parasite and inhibits complement activation in a manner functionally similar to the mammalian complement regulatory component, decay-accelerating factor. In this report, we characterized monospecific polyclonal and monoclonal antibodies which were obtained from mice and rabbits immunized with fast protein liquid chromatography-purified T-DAF. These polyclonal antibodies were shown to inhibit T-DAF activity and were capable of inducing lysis of the parasites. Both the polyclonal and monoclonal antibodies were used to screen a cDNA expression library prepared from T. cruzi trypomastigote mRNA. From this library, we obtained a partial lambda gt11 cDNA clone which showed genetic and functional similarity to the human C3 convertase inhibitor DAF (A. Nicholson-Weller, J. Burge, D. T. Fearon, P. F. Weller, and K. F. Austen, J. Immunol. 129:184-189, 1982).

This article has been cited by other articles:

• Higuchi, M. d. L., Benvenuti, L. A., Martins Reis, M., Metzger, M. (2003). Pathophysiology of the heart in Chagas' disease: current status and new developments. Cardiovasc Res 60: 96-107 [Abstract] [Full Text]  
• McConville, M. J., Mullin, K. A., Ilgoutz, S. C., Teasdale, R. D. (2002). Secretory Pathway of Trypanosomatid Parasites. Microbiol. Mol. Biol. Rev. 66: 122-154 [Abstract] [Full Text]  
• Alitalo, A., Meri, T., Ramo, L., Jokiranta, T. S., Heikkila, T., Seppala, I. J. T., Oksi, J., Viljanen, M., Meri, S. (2001). Complement Evasion by Borrelia burgdorferi: Serum-Resistant Strains Promote C3b Inactivation. Infect. Immun. 69: 3685-3691 [Abstract] [Full Text]