EARLY DEVELOPMENT AND PROGRESSION OF LYMPHOCYTE-STIMULATORY CROSS-REACTIVE IDIOTYPES EXPRESSED ON ANTIBODIES TO SOLUBLE EGG ANTIGENS DURINGSCHISTOSOMA-MANSONI INFECTION OF MICE

Citation
Sc. Bosshardt et al., EARLY DEVELOPMENT AND PROGRESSION OF LYMPHOCYTE-STIMULATORY CROSS-REACTIVE IDIOTYPES EXPRESSED ON ANTIBODIES TO SOLUBLE EGG ANTIGENS DURINGSCHISTOSOMA-MANSONI INFECTION OF MICE, European Journal of Immunology, 26(1), 1996, pp. 272-275
Citations number
22
Categorie Soggetti
Immunology
ISSN journal
00142980
Volume
26
Issue
1
Year of publication
1996
Pages
272 - 275
Database
ISI
SICI code
0014-2980(1996)26:1<272:EDAPOL>2.0.ZU;2-S
Abstract
Idiotypes (Id) that stimulate immunoregulatory anti-Id T lymphocyte pr oliferation are expressed on murine and human antibodies (Ab) to solub le egg antigens (SEA) of Schistosoma mansoni. Kinetics of early expres sion of these stimulatory Id have now been studied using immunoaffinit y-purified serum anti-SEA Ab from mice infected with S. mansoni for 6, 7, 8, 12, or 16 weeks. Rabbit anti-Id Ab specific for mouse anti-SEA Id expressed at 8 weeks post-infection (anti-8WkId) demonstrated the s trongest interactions with Id present at 7 and 8 weeks post-infection by competitive enzyme-linked immunosorbent assay. Anti-8WkId Ab reacte d progressively less well with 12WkIwd, 6WkId, and 16WkId. Splenocytes from mice infected for 8 weeks demonstrated the highest blast transfo rmation responses in vitro to anti-SEA Id from mice infected for 6 wee ks. While 7, 8, 12, and 16 weeks post-infection Id preparations stimul ated progressively less proliferation. These data indicate that althou gh eventual Id-associated immunoregulatory events contribute to chroni city in this disease, production of anti-SEA Ab that express stimulato ry cross-reactive immunoregulatory Id comprises a substantial portion of the initial, acute anti-SEA response in mice infected with Schistos oma mansoni. Furthermore, either this particular Id-expressing respons e is not maintained, or its proportional presence is greatly diminishe d by the cumulative production of other multiple anti-SEA Ab during th e establishment of chronicity, perhaps in response to its immunoregula tory influence very early in infection.