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Synthesis and secretion of immunoglobulin by spleen cells from resistant and susceptible mice infected with Trypanosoma brucei brucei GUTat 3.1
Author(s) -
NEWSON JANET,
MAHAN SUMAN M.,
BLACK SAMUEL J.
Publication year - 1990
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.1365-3024.1990.tb00942.x
Subject(s) - biology , trypanosoma brucei , epitope , antibody , spleen , secretion , virology , immunology , glycoprotein , microbiology and biotechnology , endocrinology , biochemistry , gene
Summary By 6 days after infection of susceptible C3H/He and resistant C57BL/6 mice with Trypanosoma brucei brucei GUTat 3.1, splenic plasma cell responses of both strains of mice were similar in terms of plasma cell number, intracellular Ig, Ig secretion, Ig class and Ig specificity for surface‐accessible variant surface glycoprotein (VSG) epitopes on the infecting organisms, despite higher parasitae‐mia in the C3H/He mice. By 7 days after infection, however, although splenic plasma cells from both strains of mice had greatly amplified their Ig responses, those from C57BL/6 mice (which cleared parasites from their bloodstream between 6 and 7 days after infection) contained and secreted 3–5 times more Ig specific for exposed VSG epitopes on the infecting organisms than those from C3H/He mice which did not clear parasites from their bloodstream. In vitro , trypanosomes can absorb significant amounts of VSG‐specific antibody produced by splenic plasma cells. However, differences in the detection of VSG‐specific antibodies present in, and secreted by, splenic plasma cells of 7‐day infected C3H/ He and C57BL/6 mice were shown not to result from the presence of parasites in the cultures of C3H/He spleen cells. It is argued that between 6 and 7 days after infection, the C3H/He mice selectively lose the capacity to support development of plasma cells specific for exposed VSG epitopes on the infecting organisms and that this is a consequence rather than a cause of differences in the peak levels of first wave parasitaemia.