STRONGYLOIDES-STERCORALIS - ROLE OF ANTIBODY AND COMPLEMENT IN IMMUNITY TO THE 3RD STAGE LARVAE IN BALB CBYJ MICE/

Citation
Ra. Brigandi et al., STRONGYLOIDES-STERCORALIS - ROLE OF ANTIBODY AND COMPLEMENT IN IMMUNITY TO THE 3RD STAGE LARVAE IN BALB CBYJ MICE/, Experimental parasitology, 82(3), 1996, pp. 279-289
Citations number
48
Categorie Soggetti
Parasitiology
Journal title
ISSN journal
00144894
Volume
82
Issue
3
Year of publication
1996
Pages
279 - 289
Database
ISI
SICI code
0014-4894(1996)82:3<279:S-ROAA>2.0.ZU;2-H
Abstract
Mice immunized against Strongyloides stercoralis L3 were shown to kill greater than 90% of challenge larvae contained within diffusion chamb ers. The objective of the present study was to identify the host compo nents responsible for immunity. Serum from unprotected, control mice a nd protected, immune mice in doses of 25-500 mu l was transferred into naive mice at the same time and location as larval challenge. Transfe r of as little as 50 mu l of immune serum was able to confer protectiv e immunity, The serum-transferred immunity was ablated by excluding ce lls from the larval microenvironment or by depleting granulocytes thro ugh monoclonal antibody treatment in the recipient mice. Specific anti body isotypes were isolated using protein G and isotype-specific affin ity columns. The resulting transfer experiments identified IgM as the isotype responsible for protective immunity to S. stercoralis L3. Anti body binding studies in vivo were performed and only IgM bound to the surface of infective L3 and host-derived L3 (L3(+)) in immune animals. Elevated levels of C3 were also found bound to the surface of L3/L3() in immune mice. Cobra venom factor treatment of immunized mice to de plete complement completely eliminated C3 binding to the surface of L3 /L3(+) and ablated immunity. Therefore, IgM, complement, and granulocy tes are necessary for immune elimination of S. stercoralis L3/L3(+). I dentification of antigens recognized by IgM may help select possible v accine candidates. (C) 1996 Academic Press, Inc.