Interleukin-1 (IL-1) was initially described as lymphocyte-activating factor (LAF) and endogenous pyrogen (EP) for its proinflammatory, immunostimulant, and chemotactic properties (4,5). The genes of the IL-1 complex code for three proteins: IL-1 a, IL-1P, and the IL-1 receptor antagonist (IL-1Ra). The net plasma IL-1 activity is influenced by the balance between the levels of IL-1P, the major extracellular agonist, and that of IL-1 Ra (6).
Leukemic CLL cells spontaneously produce IL-1P (7-9) and also express the IL-1P receptor (10). Although this cytokine does not induce proliferation of CLL cells, it is capable of protecting CLL lymphocytes from apoptosis, both spontaneous and induced by hydrocortisone, supporting its potential role as an autocrine survival factor in CLL (11).
However, the production of IL-1 by CLL lymphocytes correlates inversely with the stage of the disease. In fact, whereas cells from patients with stable disease have been shown to secrete near normal levels of IL-1P, B-cells from patients with progressive CLL produce lower amounts of the cytokine (12,13). Given the immunomodulatory activities of IL-1, this reduced production in progressive CLL patients might have a role in the reduced immunological control of the disease, although this aspect of the role of IL-1 in CLL has been less investigated.
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