MODULATION OF THE HOST RESPONSE IN HUMAN SCHISTOSOMIASIS .3. BLOCKING ANTIBODIES SPECIFICALLY INHIBIT IMMEDIATE HYPERSENSITIVITY RESPONSES TO PARASITE ANTIGENS

  • 1 January 1982
    • journal article
    • research article
    • Vol. 46  (4) , 777-785
Abstract
Mechanisms for modulating the host''s immune response in human schistosomiasis mansoni were described for delayed hypersensitivity responsiveness and antibody production. Since clinical symptoms of immediate hypersensitivity (i.e., allergic reactivity) are rare in schistosomiasis despite the presence of parasite-specific IgE, circulating parasite antigen and normal numbers of basophils and mast cells in infected patients, it seemed likely that there was host modulation of immediate hypersensitivity responsiveness as well. An in vitro basophil histamine release assay showed that basophils from 15 patients with Schistosoma mansoni infections are sensitized with schistosome-specific IgE and will release histamine in an antigen-dose-dependent manner when challenged with a soluble adult worm antigen. This histamine release was suppressed by autologous, but not normal, serum. Fractionation of the serum over staphylococcal protein A and antigen affinity columns identified an IgG parasite-specific blocking antibody, analogous to blocking antibodies elicited during immunotherapy of atopic patients, as being responsible for the modulation of this immediate hypersensitivity responsiveness in vitro. Blocking antibody specificity varied from patient to patient, an observation suggesting that different allergens were being recognized by different individuals. In addition to the immunoregulatory mechanisms previously described in patients with schistosome infections, there may be host modulation of immediate hypersensitivity responsiveness that appears to involve specific IgG blocking antibodies.