Toxoplasma gondii: Mechanism of resistance to complement-mediated killing

S. A. Fuhrman, Keith A Joiner

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Tachyzoites of the obligate intracellular protozoan Toxoplasma gondii are resistant to lysis in non-immune human serum. We have examined the mechanism of this serum resistance in RH and P strain organisms, which differ markedly in virulence, but are equally resistant to serum killing. Rapid, but limited, activation of the alternative complement pathway occurred in non-immune human serum, with deposition of equivalent amounts of C3 on the two strains. C component C3 bound covalently to parasite acceptor molecules via an ester linkage. The predominant form of C3 was iC3b which cannot participate in formation of a lytic C5b-9 complex. Multiple membrane constituents of the tachyzoite of T. gondii may serve as acceptors for the limited amount of C3 deposited during incubation in non-immune serum. When tachyzoites were presensitized with the lytic anti-p30 mAb 7B8, new amide-limited C3-acceptor complexes formed. Nearly equivalent C3 binding but a threefold enhancement of 125I-C9 binding occurred when mAb 7B8 pre-sensitized tachyzoites were compared to native organisms. These results indicate that tachyzoites of T. gondii are serum resistant because of failure to activate C efficiently. Presensitization with a lytic mAb alters the site of complement deposition and augments C5b-9 formation.

Original languageEnglish (US)
Pages (from-to)940-947
Number of pages8
JournalJournal of Immunology
Volume142
Issue number3
StatePublished - 1989
Externally publishedYes

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Toxoplasma
Serum
Complement Membrane Attack Complex
Complement C3b
Alternative Complement Pathway
Amides
Virulence
Esters
Parasites
Membranes

ASJC Scopus subject areas

  • Immunology

Cite this

Toxoplasma gondii : Mechanism of resistance to complement-mediated killing. / Fuhrman, S. A.; Joiner, Keith A.

In: Journal of Immunology, Vol. 142, No. 3, 1989, p. 940-947.

Research output: Contribution to journalArticle

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