INCREASED EXPRESSION OF THE INTERLEUKIN-2 (IL-2) RECEPTOR BETA-CHAIN (P70) ON CD56+ NATURAL-KILLER-CELLS AFTER INVIVO IL-2 THERAPY - P70 EXPRESSION DOES NOT ALONE PREDICT THE LEVEL OF INTERMEDIATE AFFINITY IL-2 BINDING

被引:64
作者
VOSS, SD
ROBB, RJ
WEILHILLMAN, G
HANK, JA
SUGAMURA, K
TSUDO, M
SONDEL, PM
机构
[1] UNIV WISCONSIN,DEPT PEDIAT,MADISON,WI 53792
[2] UNIV WISCONSIN,DEPT GENET,MADISON,WI 53792
[3] TOHOKU UNIV,SCH MED,DEPT MICROBIOL,SENDAI,MIYAGI 980,JAPAN
[4] DUPONT CO,GLENOLDEN LAB,GLENOLDEN,PA 19036
[5] TOKYO METROPOLITAN INST MED SCI,DEPT IMMUNOL,BUNKYO KU,TOKYO 113,JAPAN
关键词
D O I
10.1084/jem.172.4.1101
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
The expression of the 70-kD β subunit of the interleukin 2 receptor (IL2R) has been examined on peripheral blood lymphocytes (PBL) obtained from patients receiving systemic infusions of 11,2. Using monoclonal antibodies directed against p70, flow cytometric analyses revealed a greater than threefold increase in expression of the II-2R β chain on CD56+ natural killer (NK) cells from post-IL2 therapy PBL relative to pre-therapy cells. The level of p70 expression on the posttherapy cells was three- to fourfold greater (based on fluorescence intensity) than the level of p70 expression on YT cells, an NK-like cell line that expresses ~12,000 intermediate affinity IL2 binding sites/cell. Despite the high level of p70 expression, in 1251-IL2 binding assays only 790-1,290 intermediate affinity IL2 binding sites/cell were detected on post-therapy cells from six patients. These data represent the first report of increased p70 expression after in vivo 11,2 administration and suggest a requirement for at least one additional subunit for the formation of functional intermediate affinity IL2Rs. Furthermore, the presence on the surface ofpost-therapy NK cells ofexcess p70 that does not bind 11,2 with intermediate affinity implies that the formation of intermediate affinity I1r2Rs is not solely determined by the level of p70 expression, and that the response of NK cells to IL2 might be regulated by altering the expression of p70 or some other I1r2R subunit. © 1990, Rockefeller University Press., All rights reserved.
引用
收藏
页码:1101 / 1114
页数:14
相关论文
共 69 条
[1]  
ANDERSON CL, 1987, METHOD ENZYMOL, V150, P524
[2]  
BICHTHUY LT, 1987, J IMMUNOL, V139, P1550
[3]   FUNCTIONAL CONSEQUENCES OF INTERLEUKIN-2 RECEPTOR EXPRESSION ON RESTING HUMAN-LYMPHOCYTES - IDENTIFICATION OF A NOVEL NATURAL-KILLER-CELL SUBSET WITH HIGH-AFFINITY RECEPTORS [J].
CALIGIURI, MA ;
ZMUIDZINAS, A ;
MANLEY, TJ ;
LEVINE, H ;
SMITH, KA ;
RITZ, J .
JOURNAL OF EXPERIMENTAL MEDICINE, 1990, 171 (05) :1509-1526
[4]   PLASMA INTERLEUKIN-2 RECEPTOR LEVELS IN RENAL-ALLOGRAFT RECIPIENTS [J].
COLVIN, RB ;
FULLER, TC ;
MACKEEN, L ;
KUNG, PC ;
IP, SH ;
COSIMI, AB .
CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY, 1987, 43 (02) :273-276
[5]   A 2ND HUMAN INTERLEUKIN-2 BINDING-PROTEIN THAT MAY BE A COMPONENT OF HIGH-AFFINITY INTERLEUKIN-2 RECEPTORS [J].
DUKOVICH, M ;
WANO, Y ;
THUY, LTB ;
KATZ, P ;
CULLENS, BR ;
KEHRL, JH ;
GREENE, WC .
NATURE, 1987, 327 (6122) :518-522
[6]   CO-INTERNALIZATION OF THE P55 AND P70 SUBUNITS OF THE HIGH-AFFINITY HUMAN INTERLEUKIN-2 RECEPTOR - EVIDENCE FOR A STABLE TERNARY RECEPTOR COMPLEX [J].
FUNG, MR ;
JU, G ;
GREENE, WC .
JOURNAL OF EXPERIMENTAL MEDICINE, 1988, 168 (05) :1923-1928
[7]  
GOLDSTEIN D, 1989, CANCER RES, V49, P6832
[8]   THE HUMAN INTERLEUKIN-2 RECEPTOR [J].
GREENE, WC ;
LEONARD, WJ .
ANNUAL REVIEW OF IMMUNOLOGY, 1986, 4 :69-95
[9]   LYMPHOKINE-ACTIVATED KILLER CELL PHENOMENON - LYSIS OF NATURAL KILLER-RESISTANT FRESH SOLID TUMOR-CELLS BY INTERLEUKIN 2-ACTIVATED AUTOLOGOUS HUMAN PERIPHERAL-BLOOD LYMPHOCYTES [J].
GRIMM, EA ;
MAZUMDER, A ;
ZHANG, HZ ;
ROSENBERG, SA .
JOURNAL OF EXPERIMENTAL MEDICINE, 1982, 155 (06) :1823-1841
[10]  
HANK JA, 1989, J BIOL RESP MODIF, V9, P5