Shifts in the TH1/TH2 balance during human pregnancy correlate with apoptotic changes

被引:210
作者
Reinhard, G
Noll, A
Schlebusch, H
Mallmann, P
Ruecker, AV
机构
[1] Univ Bonn, Fac Med, Dept Clin Biochem, D-53105 Bonn, Germany
[2] Univ Bonn, Fac Med, Clin Obstet & Gynecol, D-53105 Bonn, Germany
[3] Univ Cologne, Fac Med, Clin Obstet & Gynecol, D-5000 Cologne 41, Germany
关键词
D O I
10.1006/bbrc.1998.8549
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
An important prerequisite for a successful pregnancy is that the maternal immune system does not reject the fetus. Down-regulation of the T helper 1 (TH1) associated cellular immune response could therefore be essential. With flow cytometric techniques, we show on a single cell level that both CD4+ and CD8+ T cells from peripheral blood produce less TH1 cytokines (i.e. IFN-gamma and IL-2) and more TH2 cytokines (i.e. IL-4) during normal human pregnancy and shortly after delivery than during non-pregnancy. The TH1/TH2 cytokine ratio in T cells of women during pregnancy and after delivery was significantly decreased. In contrast the TH1/TH2 ratio was elevated to near normal in women with recurrent spontaneous abortions, indicating a marked shift towards TH1 immunity. Fas antigen (CD95) on T cells was significantly elevated during pregnancy and in the post-delivery phase whereas the intracellular expression of anti-apoptotic protein Bcl-2 remained unchanged. Nevertheless Fas-mediated apoptosis in T cells was markedly reduced during normal human pregnancy. We hypothesize that TH1 cells undergo predominantly Fas-mediated apoptosis during pregnancy as has been shown in some TH2-prone diseases (e.g. SLE, HIV) where an elevated Fas expression on peripheral T cells is observed. This could explain the exacerbated occurrence of TH2-associated diseases in pregnancy. (C) 1998 Academic Press.
引用
收藏
页码:933 / 938
页数:6
相关论文
共 47 条
[1]  
AMASAKI Y, 1995, CLIN EXP IMMUNOL, V99, P245
[2]   P- and E-selectin mediate recruitment of T-helper-1 but not T-helper-2 cells into inflamed tissues [J].
Austrup, F ;
Vestweber, D ;
Borges, E ;
Lohning, M ;
Brauer, R ;
Herz, U ;
Renz, H ;
Hallmann, R ;
Scheffold, A ;
Radbruch, A ;
Hamann, A .
NATURE, 1997, 385 (6611) :81-83
[3]   TH1 AND TH2 CYTOKINE PRODUCTION BY PERIPHERAL-BLOOD MONONUCLEAR-CELLS FROM HIV-INFECTED PATIENTS [J].
BARCELLINI, W ;
RIZZARDI, GP ;
BORGHI, MO ;
FAIN, C ;
LAZZARIN, A ;
MERONI, PL .
AIDS, 1994, 8 (06) :757-762
[4]   PLACENTA AS AN IMMUNOLOGICAL BARRIER [J].
BEER, AE ;
SIO, JO .
BIOLOGY OF REPRODUCTION, 1982, 26 (01) :15-27
[5]   CD28 AND APOPTOSIS [J].
BOISE, LH ;
NOEL, PJ ;
THOMPSON, CB .
CURRENT OPINION IN IMMUNOLOGY, 1995, 7 (05) :620-625
[6]  
CARTER LL, 1995, J IMMUNOL, V155, P1028
[7]  
Check JH, 1997, AM J REPROD IMMUNOL, V37, P330
[8]  
Check JH, 1996, AM J REPROD IMMUNOL, V35, P277
[9]   VIRUS-SPECIFIC CD8(+) CELLS CAN SWITCH TO INTERLEUKIN-5 PRODUCTION AND INDUCE AIRWAY EOSINOPHILIA [J].
COYLE, AJ ;
ERARD, F ;
BERTRAND, C ;
WALTI, S ;
PIRCHER, H ;
LEGROS, G .
JOURNAL OF EXPERIMENTAL MEDICINE, 1995, 181 (03) :1229-1233
[10]   GENERATION OF POLARIZED ANTIGEN-SPECIFIC CD8 EFFECTOR POPULATIONS - RECIPROCAL ACTION OF INTERLEUKIN (IL)-4 AND IL-12 IN PROMOTING TYPE-2 VERSUS TYPE-1 CYTOKINE PROFILES [J].
CROFT, M ;
CARTER, L ;
SWAIN, SL ;
DUTTON, RW .
JOURNAL OF EXPERIMENTAL MEDICINE, 1994, 180 (05) :1715-1728