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Oxidative Burst in Human Epstein‐Barr Virus‐Transformed B‐Cell Lines Triggered by Immobilized Specific Antigen
Author(s) -
MALY F.E.,
URWYLER A.,
TENGLER R.,
STEINITZ M.,
GOLDING B.,
WECK A. L.
Publication year - 1990
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.1990.tb03208.x
Subject(s) - antigen , microbiology and biotechnology , respiratory burst , antibody , superoxide , nadph oxidase , chemistry , cell culture , immunoglobulin g , lucigenin , biology , reactive oxygen species , biochemistry , immunology , enzyme , genetics
Normal human B lymphocytes and Epstein‐Barr virus‐transformed B‐cell lines can produce reactive oxygen species such as superoxide if treated with phorbol myristate acetate (PMA) or with the surface immunoglobulin cross‐linking agents protein A and anti‐immunoglobulin. Here, we investigated under which conditions specific antigen, the natural ligand of surface immunoglobulin, can stimulate an oxidative burst in monoclonal Epstein Barr virus‐transformed B‐cell lines producing antibodies of known specificities. After a short lag time of 1‐2 min, exposure to the specific antigen stimulated a prolonged oxidative burst ( t max , 30‐90 min). as measured by Lucigenin‐enhanced, superoxide dismutase‐inhibitable chemiluminescence, in the corresponding line only. The effect was induced in each line if the specific antigen was immobilized to a solid support. Except in one line in which antigen also stimulated an oxidative burst if presented at relatively high density on a soluble carrier, soluble antigen did not induce B‐cell oxidase activation. This suggests that normal, non‐transformed B lymphocytes also require interaction with relatively dense deposits of specific antigen for activation of their oxidase.