Rapid expulsion of Trichinella spiralis in adult rats mediated by monoclonal antibodies of distinct IgG isotypes.

  • 1 March 1992
    • journal article
    • Vol. 75  (3) , 520-7
Abstract
The role of IgG in rapid expulsion of Trichinella spiralis in adult rats was analysed. In this experimental model, rats were first infected with an unrelated nematode Heligmosomoides polygyrus, then 5-14 days later, immune serum, its fractions, or IgG monoclonal antibody (mAb) was transferred. Rats were challenged with T. spiralis muscle larvae 24 hr after antibody transfer and intestinal worms counted at various times, up to 24 hr, after challenge. Provided rats were exposed to H. polygyrus first, immune serum, affinity chromatography-isolated immune IgE, IgE-depleted immune serum, or monoclonal antibodies of IgG1, IgG2a and IgG2c isotypes were all able to transfer rapid expulsion. Protection varied from 40 to greater than 90% larval T. spiralis rejection and was dose dependent, requiring, for IgG1, a minimum of 5 mg of transferred protein. Antibody specificity was predominantly against the dominant larval secreted/cuticular antigen TSL-1 for IgE and was exclusively so for the mAb. A comparison of quantitative differences in effective amounts of transferred antibody as well as the distinct priming requirements suggest that IgE functions through an intestinal mechanism that is different from that for IgG1 and IgG2c. Whether or not IgG2a functions homocytotropically, or as the other IgG has not been resolved. Since neither the T-helper (Th) cell transfer or the H. polygyrus form of intestinal priming confers protection by itself, these data suggest that rapid expulsion is predominantly an antibody-mediated process albeit with a required intestinal element. The results support earlier data in showing that two steps are required for rapid expulsion to be expressed and this is so for both IgE- and IgG-mediated mechanisms. Finally, the results show that IgG of various isotypes and IgE have a functional role in the expression of intestinal immunity.

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