Premium
B‐cell chronic lymphocytic leukaemia cells express and release transforming growth factor‐β
Author(s) -
Kremer JeanPierre,
Reisbach Gilbert,
Nerl Christoph,
Döurmer Peter
Publication year - 1992
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1992.tb04561.x
Subject(s) - haematopoiesis , autocrine signalling , cd19 , biology , transforming growth factor , peripheral blood mononuclear cell , b cell , population , progenitor cell , growth factor , secretion , immunology , cancer research , cell culture , microbiology and biotechnology , stem cell , endocrinology , in vitro , antibody , medicine , receptor , biochemistry , genetics , environmental health
Summary Transforming growth factor‐β (TGF‐β) has been described as a potent inhibitor of various cell types, among others of primitive haematopoietic progenitors in vitro, and as a negative autocrine regulator of normal B lymphocyte growth and differentiation. In the present study we investigated TGF‐β gene expression in peripheral blood mononuclear cells (PBMC) and in B cells from patients with B‐cell chronic lymphocytic leukaemia (B‐CLL) and from normal controls. Monocyte depleted B‐CLL cells expressed constitutively mRNA for TGF‐β1 and secreted low amounts of TGF‐β activity into the culture medium. Stimulation of cells by phorbol ester noticeably enhanced mRNA levels as well as protein secretion in most cases. TGF‐β activity was of the same magnitude as in normal controls. We next analysed TGF‐β in highly enriched B lymphocytes from B‐CLL (95100% CD19+), and found that TGF‐β secretion was up to 3 times higher than in the original PBMC population. It is discussed that B‐CLL cells might escape from negative regulation by TGF‐β and, on the other hand, inhibit normal haematopoietic cell proliferation and thereby achieve a growth advantage in the haematopoietic tissues.