Role of human decay-accelerating factor in the evasion of Schistosoma mansoni from the complement-mediated killing in vitro [published erratum appears in J Exp Med 1992 Feb 1;175(2):619]

doi:10.1084/jem.174.6.1399

This Article

	Full Text (PDF, 953K)
	Alert me when this article is cited
	Citation Map

Services

	Email this article
	Similar articles in this journal
	Similar articles in PubMed
	Alert me to new content in the JEM
	Download to citation manager

Citing Articles

	Citing Articles via HighWire
	Citing Articles via CrossRef
	Citing Articles via Google Scholar

Google Scholar

	Articles by Horta, M. F.
	Articles by Fatima M$[corrected to Horta, M.
	Search for Related Content

PubMed

	PubMed Citation
	Articles by Horta, M. F.
	Articles by Fatima M$[corrected to Horta, M.


Social Bookmarking

	What's this?

ARTICLES

Role of human decay-accelerating factor in the evasion of Schistosoma mansoni from the complement-mediated killing in vitro [published erratum appears in J Exp Med 1992 Feb 1;175(2):619]

MF Horta, FJ Ramalho-Pinto and MF] Fatima M$[corrected to Horta
Department of Biochemistry-Immunology, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.

Decay-accelerating factor (DAF) is a 70-kD membrane glycoprotein that prevents complement (C)-mediated hemolysis by blocking the assembly or accelerating the decay of C3 convertase. Purified DAF is known to incorporate into the membrane of DAF-deficient cells, inhibiting lysis. Since Schistosoma mansoni is a blood-dwelling parasite, we investigated whether DAF can be transferred from human erythrocytes to the worm and protect it against C-mediated killing in vitro. We have found that schistosomula (schla) incubated with normal human erythrocytes (N-HuE), but not with DAF-deficient erythrocytes, become resistant to C damage in vitro. Protected parasites acquire a 70-kD surface protein which can be immunoprecipitated by anti-DAF antibodies. The acquired resistance is abrogated by treatment of N-HuE-incubated parasites with anti-DAF antibody. These results indicate that, in vitro, N-HuE DAF can be transferred to schla, and suggest its participation in preventing their C-mediated killing. This could represent an important strategy of parasites to evade the host's immune response in vivo.
Add to CiteULike CiteULike Add to Complore Complore Add to Connotea Connotea Add to Del.icio.us Del.icio.us Add to Digg Digg Facebook Add to Reddit Reddit Add to Technorati Technorati Twitter What's this?

This article has been cited by other articles:

Inal, J. M., Hui, K.-M., Miot, S., Lange, S., Ramirez, M. I., Schneider, B., Krueger, G., Schifferli, J.-A. (2005). Complement C2 Receptor Inhibitor Trispanning: A Novel Human Complement Inhibitory Receptor. J. Immunol. 174: 356-366 [Abstract] [Full Text]
La Flamme, A. C., MacDonald, A. S., Huxtable, C. R., Carroll, M., Pearce, E. J. (2003). Lack of C3 Affects Th2 Response Development and the Sequelae of Chemotherapy in Schistosomiasis. J. Immunol. 170: 470-476 [Abstract] [Full Text]
Loukas, A., Jones, M. K., King, L. T., Brindley, P. J., McManus, D. P. (2001). Receptor for Fc on the Surfaces of Schistosomes. Infect. Immun. 69: 3646-3651 [Abstract] [Full Text]
Rautemaa, R., Jarvis, G. A., Marnila, P., Meri, S. (1998). Acquired Resistance of Escherichia coli to Complement Lysis by Binding of Glycophosphoinositol-Anchored Protectin (CD59). Infect. Immun. 66: 1928-1933 [Abstract] [Full Text]
Camacho-Lobato, L., Borges, D. R. (1996). Plasma Proteins of Hemostasis in the Hepatointestinal Form of Schistosomiasis Mansoni. CLIN APPL THROMB HEMOST 2: 276-278 [Abstract]