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Proliferation of the BCL1 B cell lymphoma induced by IL‐4 and IL‐5 is dependent on IL‐6 and GM‐CSF
Author(s) -
NI KEPING,
O'NEILL HELEN C.
Publication year - 1992
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/icb.1992.40
Subject(s) - lymphokine , autocrine signalling , cell growth , biology , interleukin 3 , colony stimulating factor , growth factor , granulocyte macrophage colony stimulating factor , microbiology and biotechnology , in vitro , immunology , cytokine , receptor , t cell , haematopoiesis , stem cell , il 2 receptor , biochemistry , immune system
Summary Lymphokine requirements for the in vitro proliferation of the spleen‐dependent B cell lymphoma BCL1 have been analysed. Cells were found to respond by proliferation to added recombinant (r) interleukin‐4 (IL‐4), r‐IL‐5 and recombinant granulocyte‐macrophage colony‐stimulating factor (r‐GM‐CSF). Inhibition by antibodies specific for each of these lymphokines has confirmed growth factor‐dependent growth. Anti‐GM‐CSF has, however, been found to inhibit the proliferation of BCL1 cells induced by r‐IL‐4 and r‐IL‐5, as well as r‐GM‐CSF, suggesting that BCLI cells may express receptors for GM‐CSF and that GM‐CSF may be able to act synergistically with IL‐4 and IL‐5 in promoting cell proliferation. Anti‐IL‐6 antibody was also found to be a very effective inhibitor of BCL1 proliferation induced by either IL‐4 or IL‐5 but not by GM‐CSF. Added IL‐6 did not stimulate BCL1 proliferation, suggesting that endogenous IL‐6 may regulate the autocrine growth of BCL1 cells. BCL1 cell proliferation in vitro appears to be regulated by interactions between multiple growth factors.