Premium
Immune‐recognition of Schistosoma mansoni primary sporocysts may require specific receptors on Biomphalaria glabrata hemocytes
Author(s) -
BAYNE C. J.,
LOKER E. S.,
YUI MARYA.,
STEPHENS JENNIFER A.
Publication year - 1984
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/j.1365-3024.1984.tb00822.x
Subject(s) - biomphalaria glabrata , schistosoma mansoni , antigen , biology , antibody , snail , immune system , biomphalaria , immunology , antiserum , immunoglobulin g , receptor , schistosoma , microbiology and biotechnology , schistosomiasis , helminths , biochemistry , ecology
Summary Cellular interactions, leading to cell‐mediated cytotoxicity when Biomphalaria glabrata hemocytes encapsulate Schistosoma mansoni sporocysts, have been investigated. Rabbit antibodies (IgG), when bound to antigens on sporocyst surfaces, prevent the normal cytoadherence (CA) of hemocytes from both susceptible and resistant host snails. Since interference with CA occurs with even fixed sporocysts, the effect is not due to IgG stimulated modulation of the parasite surface. Using two antisera with some overlapping specificities, and quantitative immunofluorescent antibody technique (QIFAT), we determined the concentrations of IgG needed to place equivalent amounts of IgG on the sporocysts. At these concentrations, CA was affected differentially, implying that interference was due to the specific antigens bound, and not due simply to the presence of IgG. Also with QIFAT we determined how much F(ab')2 and IgG from anti‐sporocyst serum were needed to block an equivalent amount of antigenic determinants from access by whole FITC labelled IgG. Sporocysts whose surface antigens were equally blocked were equally unadherent for hemocytes, supporting the notion that the nature of obscured antigens, and neither the Fc portion nor the larger size of intact IgG protein, was responsible for the effect on CA. These surprising results imply a role for specific antigen binding sites on snail hemocytes.