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Research Article Free access | 10.1172/JCI113748

Interleukin 1-dependent paracrine granulopoiesis in chronic granulocytic leukemia of the juvenile type.

G C Bagby Jr, C A Dinarello, R C Neerhout, D Ridgway, and E McCall

Medical Research Service, Veterans Administration Medical Center, Portland, Oregon 97201.

Find articles by Bagby, G. in: PubMed | Google Scholar

Medical Research Service, Veterans Administration Medical Center, Portland, Oregon 97201.

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Medical Research Service, Veterans Administration Medical Center, Portland, Oregon 97201.

Find articles by Neerhout, R. in: PubMed | Google Scholar

Medical Research Service, Veterans Administration Medical Center, Portland, Oregon 97201.

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Medical Research Service, Veterans Administration Medical Center, Portland, Oregon 97201.

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Published October 1, 1988 - More info

Published in Volume 82, Issue 4 on October 1, 1988
J Clin Invest. 1988;82(4):1430–1436. https://doi.org/10.1172/JCI113748.
© 1988 The American Society for Clinical Investigation
Published October 1, 1988 - Version history
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Abstract

Marrow and peripheral blood cells from nine children with juvenile chronic granulocytic leukemia (JCGL) demonstrated intense (94 +/- 16% maximum) spontaneous granulocyte/macrophage colony growth but cells from five children with the adult variety of CGL did not. This unusual pattern of colony growth depended upon a stimulatory protein(s) produced by mononuclear phagocytes. No GM-CSA activity was found in any chromatofocused fraction of JCGL monocyte-conditioned media but an activity that induced GM-CSA in umbilical vein endothelial cells was detected at pI 6.9-7.2. Moreover, the CSA-inducing monokine was neutralized by an anti-IL-1 antibody in vitro and, in the one case so tested, the same antibody also inhibited "spontaneous" colony growth. Therefore granulocyte/macrophage colony growth in JCGL is characteristically abnormal and distinguishes JCGL from the adult form of the disease. This abnormality depends upon the production, by mononuclear phagocytes, of IL-1 which, in turn, stimulates the release of high levels of colony stimulating activity by other cells. The high proliferative activity of CFU-GM we found in JCGL patients, and the high levels of GM-CSA found in their serum are compatible with the view that the in vitro abnormality reflects a similar abnormality in vivo.

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