GENES FOR INTERLEUKIN-7 ARE TRANSCRIBED IN LEUKEMIC-CELL SUBSETS OF INDIVIDUALS WITH CHRONIC LYMPHOCYTIC-LEUKEMIA

被引:50
作者
FRISHMAN, J
LONG, B
KNOSPE, W
GREGORY, S
PLATE, J
机构
[1] RUSH PRESBYTERIAN ST LUKES MED CTR,DEPT MED,MED ONCOL SECT,1753 W CONGRESS PKWY,CHICAGO,IL 60612
[2] RUSH PRESBYTERIAN ST LUKES MED CTR,DEPT IMMUNOL,CHICAGO,IL 60612
[3] RUSH PRESBYTERIAN ST LUKES MED CTR,DEPT MED,HEMATOL SECT,CHICAGO,IL 60612
关键词
D O I
10.1084/jem.177.4.955
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Regulation of expression of interleukin 7 (IL-7) mRNA is aberrant in the leukemic subset of cells of chronic lymphocytic leukemia (CLL) patients. The entire coding sequence for IL-7 as well as an alternatively spliced IL-7 mRNA are transcribed in these leukemic cells. No IL-7 mRNA expression is detected in fresh peripheral blood mononuclear cells from normal individuals. Furthermore, the ''normal'' nonleukemic subsets of cells isolated from the same CLL patients also do not express IL-7 mRNA. The only subset of cells in which IL-7 mRNA is detected is the one that contains the leukemic cells themselves. The polymerase chain reaction was used to examine cytokine expression, and flow cytometry was used to purify the various subsets of peripheral blood mononuclear cells examined in these studies, as well as to examine IL-7 receptor expression. A proportion of the cells from the CLL patients express receptors that are capable of binding IL-7, whereas T cell-depleted normal cell preparations do not express receptors for IL-7 that are detectable with IL-7 fluorokines. The IL-7 receptor-bearing cells in CLL patients include a portion of leukemic cells and a fraction of the T cells, as well as some non-T, non-B cells. These findings suggest that IL-7 and IL-7 receptor expression in CLL may be relevant not only to growth regulation of the leukemic cells but to the immunological abnormalities that occur in the disease as well, possibly via the induction of inappropriate immune activity of IL-7 receptor-bearing cells.
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页码:955 / 964
页数:10
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