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B Bonnel

Publications and source records attributed to B Bonnel.

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Tolerance in rats by transplacental transfer of Dipetalonema viteae microfilariae: recognition of putative tolerogen(s) by antibodies that inhibit antigen-specific lymphocyte proliferation.

We have previously reported (Nature 1982. 299:361) that the transplacental transfer of Dipetalonema viteae microfilariae (mf) can induce an antigen-specific tolerance in rats. Rats thus tolerized have serum factor(s) which block(s) antigen-specific lymphocyte proliferation. The results of experiments involving fractionation of antisera from tolerant animals indicate that the inhibitory activity for antigen-specific blastogenesis resides in IgG antibodies. Absorption of IgG (eluted from protein A) with specific filarial antigens reduced the inhibition from 58% to 9% whereas a similar immunosorption of IgG size fraction (obtained by applying to AcA 34 Ultrogel) resulted in a decrease from 72% to 35%. This suggests that IgG size fraction might include factor(s) derived from mf and was partially blocking the blastogenic response. Since the tolerant animals harbor only mf, we have used radiolabeled mf surface antigens for immunoprecipitation by antisera from tolerant animals. Antibodies from tolerant animals have a different specificity for filarial antigens compared to those from immunocompetent and mf-resistant rats.

Animals

Platelet mediated killing of larvae from different filarial species in the presence of Dipetalonema viteae stimulated IgE antibodies.

The platelets from normal rats interact with microfilariae of Dipetalonema viteae in vitro in the presence of antibodies leading to the killing of the parasite. The antibody involved in this reaction is identified as IgE because the absorption of immune rat serum on anti-rat IgE column or the pretreatment of platelets with anti-Fc epsilon receptor resulted in a significant reduction in the percentage of killing of microfilariae. This antibody, which mediates platelet activity towards microfilariae, appears early in the secondary infection and persists for a short period of time. This short-lasting IgE antibody is not apparently present in the form of large complexes since the supernatant but not the pellet after ultracentrifugation was able to mediate killing of microfilariae by platelets. IgE-dependent platelet-mediated parasite killing is neither stage- nor species-specific because the microfilariae (LI) of Brugia malayi or of Loa loa and infective larvae (L3) of D. viteae or of B. malayi were killed when they were incubated with the serum obtained from rats at day 8 after secondary infection with adult D. viteae worms. The results of the present study suggest that platelets can actively participate in the immunological killing of filarial larvae.

Animals