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Burkitt's cells can be triggered by teleocidin to secrete interferon‐γ
Author(s) -
Benjamin David,
Hartmann Dan P.,
Bazar Leonard S.,
Jacobson Robert J.
Publication year - 1986
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830220207
Subject(s) - secretion , interferon , biology , cell culture , cytokine , microbiology and biotechnology , immunology , endocrinology , genetics
Abstract The secretion of interferon (IFN)‐γ by T lymphocytes is mediated by the synthesis of interleukin 2 (IL‐2) and the availability of IL‐2 receptors. Since some Burkitt's lymphoma lines express Tac antigen and can be triggered to secrete IL‐2 following activation with the new tumor promoter teleocidin, we addressed the question of whether the induction of IL‐2 by B lymphocytes is accompanied by the induction of IFN‐γ. IFN‐γ has not been detected in any of the 25 cell lines studied, and following stimulation with teleocidin, we triggered the synthesis of IFN‐γ in JLP(C), a pre‐Burkitt's cell line. The mechanism of IFN‐γ secretion by B lymphocytes is not clear. Our findings demonstrate that the synthesis of IL‐2 by B cells is not accompanied by IFN‐γ and suggest that the synthesis of IFN‐γ is not mediated by IL‐2 or IL‐1 or B‐cell growth factor. Neutralization studies have shown that IFN‐γ secretion is not accompanied by the induction of IFN‐α or IFN‐β. Our data imply that B cells can be triggered to secrete IFN‐γ under certain circumstances. Whether similar function occurs in vivo is not known.