GRANULOCYTE-COLONY-STIMULATING FACTOR INDUCES INCREASED SERUM LEVELS OF SOLUBLE INTERLEUKIN-2 RECEPTORS PRECEDING ENGRAFTMENT IN AUTOLOGOUS BONE-MARROW TRANSPLANTATION

被引:11
作者
DREGER, P [1 ]
GRELLE, K [1 ]
ECKSTEIN, V [1 ]
SUTTORP, M [1 ]
MULLERRUCHHOLTZ, W [1 ]
LOFFLER, H [1 ]
SCHMITZ, N [1 ]
机构
[1] UNIV KIEL,INST IMMUNOL,W-2300 KIEL 1,GERMANY
关键词
D O I
10.1111/j.1365-2141.1993.tb04623.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The serum levels of soluble interleukin 2 receptors (sIL-2R) were determined in 19 patients who received high-dose chemotherapy and an autologous or syngeneic bone marrow transplant (BMT) for treatment of Hodgkin's disease (n = 18) or non-Hodgkin's lymphoma (n = 1). Twelve patients received granulocyte colony-stimulating factor (G-CSF) from day 0 or day + 1 after autologous BMT until the white blood cell count had been stable for 9 d above 1 x 10(9)/l, the remaining seven patients did not receive growth factors. In all G-CSF-treated patients the sIL-2R levels increased steadily in the early post-transplant course, even in the absence of infection. This increase was statistically significant 2-4 d prior to the appearance of leucocytes in the peripheral blood (median 340 pM versus median 256 pM immediately after BMT, P < 0.025) and peaked with the appearance of first peripheral blood leucocytes (median 536 pm, P < 0.001). Cessation of G-CSF administration resulted in a decline of sIL-2R levels. In contrast, five of seven patients without G-CSF treatment did not exhibit an sIL-2R increase before or at the time of engraftment. Infection was associated with a rise of sIL-2R levels. A correlation between sIL-2R levels and total leucocyte count, lymphocyte count, or CD25 + lymphocyte count was not evident. These data suggest that after autologous BMT G-CSF induces increased sIL-2R levels, which occur independent of lymphocyte activation. This may be compatible with involvement of immature bone marrow cells in G-CSF-induced sIL-2R release.
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页码:7 / 13
页数:7
相关论文
共 26 条
[1]   CERTAIN MYELOID CELLS POSSESS RECEPTORS FOR INTERLEUKIN-2 [J].
ARMITAGE, RJ ;
LAI, AP ;
ROBERTS, PJ ;
CAWLEY, JC .
BRITISH JOURNAL OF HAEMATOLOGY, 1986, 64 (04) :799-807
[2]   REGULATION OF EXPRESSION OF THE INTERLEUKIN-2 RECEPTOR ON HEMATOPOIETIC-CELLS BY INTERLEUKIN-3 [J].
BIRCHENALLSPARKS, MC ;
FARRAR, WL ;
RENNICK, D ;
KILIAN, PL ;
RUSCETTI, FW .
SCIENCE, 1986, 233 (4762) :455-458
[3]  
CIMINO G, 1991, LEUKEMIA, V5, P32
[4]  
FAISAL M, 1990, BLOOD, V76, P1580
[5]  
GANSER A, 1989, BLOOD, V73, P31
[6]  
HANCOCK WW, 1988, J IMMUNOL, V140, P3021
[7]   EXPRESSION OF INTERLEUKIN-2 RECEPTORS AND BINDING OF INTERLEUKIN-2 BY GAMMA INTERFERON INDUCED HUMAN-LEUKEMIC AND NORMAL MONOCYTIC CELLS [J].
HERRMANN, F ;
CANNISTRA, SA ;
LEVINE, H ;
GRIFFIN, JD .
JOURNAL OF EXPERIMENTAL MEDICINE, 1985, 162 (03) :1111-1116
[8]  
HO AD, 1990, BLOOD, V75, P203
[9]  
HOLTER W, 1987, J IMMUNOL, V138, P2917
[10]   DETECTION AND FUNCTIONAL-STUDIES OF P60-65 (TAC ANTIGEN) ON ACTIVATED HUMAN B-CELLS [J].
JUNG, LKL ;
HARA, T ;
FU, SM .
JOURNAL OF EXPERIMENTAL MEDICINE, 1984, 160 (05) :1597-1602