Differential expression of proteinase inhibitor-9 and granzyme B mRNAs in activated immunocompetent cells

被引:6
作者
Horie, O
Saigo, K
Murayama, T
Ryo, R
机构
[1] Kobe Univ, Sch Med, Dept Med Technol, Fac Hlth Sci, Kobe, Hyogo 6540142, Japan
[2] Kobe Univ Hosp, Div Blood Transfus, Kobe, Hyogo, Japan
[3] Hyogo Med Ctr Adults, Div Hematol Oncol, Dept Med, Akashi, Hyogo, Japan
关键词
PI-9; granzyme B; cytokine; GVHD; real-time quantitative PCR;
D O I
10.1620/tjem.205.103
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
HORIE. O., SAIGO. K., MURAYAMA, T. and Ryo, R. Differential Expression of Proteinase Inhibitor-9 and Granzyme B mRMAs in Activated Immunocompetent Cells. Tohoku J. Exp. Med., 2005, 205 (2) 103-113 - The role of proteinase inhibitor (PI)-9 in hematopoietic cells remains unclear. To clarify the role of PI-9 in these cells. we compared the expressions of PI-9 mRNA and antigen with those of granzyme B (GrB). While the strongest expression of PI-9 mRNA was observed in a NK cell line YT-N10, it was also expressed in a B-acute lymphoblastic leukemia cell line U-Tree02. an Epstein-Barr Virus (EBV)-transformed B cell clone. a CD8(+) T lymphocyte clone and a megakaryocytic cell line CMK. but not in a T cell line Jurkat. Phorbol 12-myristate 13 acetate (PMA) enhanced PI-9 mRNA expression in the CD8(+) T lymphocyte clone and YT-N10 cells prior to GrB mRNA expression. IL-2 and IL-12 also had similar effects. PMA increased PI-9 mRNA expression in the EBV-transformed B cell clone and CMK cells. but IL-6 showed no effect. No chances were noted in PI-9 and GrB antigens after the addition of these agonists. Patients with graft-versus-host disease (GVHD) may have activated CTLs and NK cells. We therefore examined the expression of PI-9 and GrB mRNAs in eight patients after allogeneic hematopoietic stern cell transplantation with GVHD (n = 4) or without chronic GVHD (n = 4). Expression of GrB mRMA was significantly increased in three patients with GVHD and one patient without GVHD. Surprisingly, PI-9 mRNA expression was decreased in the eight patients. These results indicate that earlier synthesis of PI-9 may be essential for the prevention of autolysis of immunocompetent cells. and that the expression of PI-9 and GrB mRNAs may be controlled through different pathways. PI-9; granzyme B; cytokine; GVHD; real-time quantitative PCR (C) 2005 Tohoku University Medical Press
引用
收藏
页码:103 / 113
页数:11
相关论文
共 31 条
[1]   THE ROLE OF HUMAN INTERLEUKIN-6 IN B-CELL ISOTYPE REGULATION AND DIFFERENTIATION [J].
BERTOLINI, JN ;
BENSON, EM .
CELLULAR IMMUNOLOGY, 1990, 125 (01) :197-209
[2]   STABLE GROWTH TRANSFORMATION OF HUMAN LYMPHOCYTES-T BY HERPESVIRUS SAIMIRI [J].
BIESINGER, B ;
MULLERFLECKENSTEIN, I ;
SIMMER, B ;
LANG, G ;
WITTMANN, S ;
PLATZER, E ;
DESROSIERS, RC ;
FLECKENSTEIN, B .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (07) :3116-3119
[3]   Selective regulation of apoptosis: the cytotoxic lymphocyte serpin proteinase inhibitor 9 protects against granzyme B-mediated apoptosis without perturbing the Fas cell death pathway [J].
Bird, CH ;
Sutton, VR ;
Sun, JR ;
Hirst, CE ;
Novak, A ;
Kumar, S ;
Trapani, JA ;
Bird, PI .
MOLECULAR AND CELLULAR BIOLOGY, 1998, 18 (11) :6387-6398
[4]   The granzyme B inhibitor, protease inhibitor 9, is mainly expressed by dendritic cells and at immune-privileged sites [J].
Bladergroen, BA ;
Strik, MCM ;
Bovenschen, N ;
van Berkum, O ;
Scheffer, GL ;
Meijer, CJLM ;
Hack, CE ;
Kummer, JA .
JOURNAL OF IMMUNOLOGY, 2001, 166 (05) :3218-3225
[5]   The granzyme B inhibitor, PI-9, is present in endothelial and mesothelial cells, suggesting that it protects bystander cells during immune responses [J].
Buzza, MS ;
Hirst, CE ;
Bird, CH ;
Hosking, P ;
McKendrick, J ;
Bird, PI .
CELLULAR IMMUNOLOGY, 2001, 210 (01) :21-29
[6]   NORMAL FUNCTIONAL-CHARACTERISTICS OF CULTURED HUMAN PROMYELOCYTIC LEUKEMIA-CELLS (HL-60) AFTER INDUCTION OF DIFFERENTIATION BY DIMETHYLSULFOXIDE [J].
COLLINS, SJ ;
RUSCETTI, FW ;
GALLAGHER, RE ;
GALLO, RC .
JOURNAL OF EXPERIMENTAL MEDICINE, 1979, 149 (04) :969-974
[7]   INTERLEUKIN-2 ACTIVATED HUMAN KILLER LYMPHOCYTES - LACK OF INVOLVEMENT OF INTERFERON IN THE DEVELOPMENT OF IL-2-ACTIVATED KILLER LYMPHOCYTES [J].
DAMLE, NK ;
DOYLE, LV .
INTERNATIONAL JOURNAL OF CANCER, 1987, 40 (04) :519-524
[8]  
Das H, 2000, BRIT J CANCER, V82, P1682
[9]   IL-12 SYNERGIZES WITH IL-2 TO INDUCE LYMPHOKINE-ACTIVATED CYTOTOXICITY AND PERFORIN AND GRANZYME GENE-EXPRESSION IN FRESH HUMAN NK CELLS [J].
DEBLAKERHOHE, DF ;
YAMAUCHI, A ;
YU, CR ;
HORVATHARCIDIACONO, JA ;
BLOOM, ET .
CELLULAR IMMUNOLOGY, 1995, 165 (01) :33-43
[10]   REGULATION OF HUMAN CYTOLYTIC LYMPHOCYTE-RESPONSES BY INTERLEUKIN-12 [J].
GATELY, MK ;
WOLITZKY, AG ;
QUINN, PM ;
CHIZZONITE, R .
CELLULAR IMMUNOLOGY, 1992, 143 (01) :127-142