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Interleukin‐1 and tumor necrosis factor production in acute non‐lymphoid leukemia
Author(s) -
Erroi Annalaura,
Specchia Giorgina,
Liso Vincenzo,
Colotta Francesco,
Bersani Laura,
Polentarutti Nadia,
ZhenGuo Chen,
Allavena Paola,
Mantovani Alberto
Publication year - 1989
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/j.1600-0609.1989.tb00241.x
Subject(s) - cytokine , tumor necrosis factor alpha , leukemia , immunology , lipopolysaccharide , biology , stimulation , cancer research , endocrinology
We have investigated interleukin‐1 (IL‐1) and tumor necrosis factor (TNF) release in 20 patients with acute non‐lymphoid leukemia (ANLL) after culture with bacterial lipopolysaccharide (LPS) or in the absence of deliberate stimulation. IL‐1 and TNF were identified by appropriate bioassays inhabitable by specific antibodies. The capacity to produce IL‐1 was expressed by most ANLL cases investigated irrespective of the FAB (French, American, British) subtype. However, the M4 and M5 cases tended to be better producers of IL‐1 than M1‐M3 cases. In contrast, TNF release was only restricted to M5 leukemias (3 out of 4 cases examined). Cytokine production may therefore provide additional criteria for a functional classification of ANLL. A considerable proportion of ANLL cases (7/18 bone marrow samples and 12/20 blood samples) released appreciable quantities of IL‐1 in culture in the absence of deliberate stimulation. “Spontaneous” TNF production was also detected in 1 out of 3 MS cases. Cells were cultured under LPS‐negative conditions and polymixin B did not affect spontaneous cytokine release. Moreover, Northern blot analysis showed that freshly isolated, non‐cultured ANLL cells expressed IL‐1 β transcripts. Inasmuch as IL‐1 is responsible for hemopoietin‐1 activity and IL‐1 induces colony stimulating factor production in various cell types, the observation of IL‐1 production in ANLL suggests that this mediator may be involved in regulatory amplifying circuits of leukemic cell proliferation.