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Evidence for a paracrine pathway of B‐cell stimulation in hairy cell leukaemia
Author(s) -
SCHMID MATHIAS,
SCHREZENMEIER HUBERT,
STAIB G.,
PORZSOLT FRANZ
Publication year - 1995
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.1365-2141.1995.tb03394.x
Subject(s) - autocrine signalling , paracrine signalling , hairy cell , clone (java method) , cell growth , biology , hairy cell leukemia , cytokine , growth factor , cancer research , tumor necrosis factor alpha , immunology , cell culture , receptor , leukemia , biochemistry , dna , genetics
It is a well‐known phenomenon that the growth of malignant B‐lymphocytes, i.e. hairy cells, is regulated by cytokines. Several investigators have suggested that the stimulating cytokines are produced by the malignant B cells themselves, indicating an autocrine growth regulation. In this paper we demonstrate that T‐lymphocyte clones produce soluble mediators which stimulate the growth of malignant B lymphocytes. The incidence of the growth‐stimulating T‐cell clones derived from peripheral blood is identical in patients with hairy cell leukaemia (HCL) and healthy controls. About 50% of the clones stimulate the growth of hairy cells, but not the growth of purified B lymphocytes of healthy donors. The stimulating activity of a single clone varies when tested on different hairy cells. Interferon alpha (IFNa), but not antibodies against tumour necrosis factor alpha (TNFQ) or interleukin‐2 (IL‐2), completely inhibit the growth‐stimulating activity. Our results indicate that a paracrine growth regulation has to be considered in addition to the postulated autocrine loop in the growth regulation of malignant B cells.