Effects of intravenous immunoglobulin in vivo on abnormally increased tumor necrosis factor-alpha activity in human immunodeficiency virus type 1 infection

被引:18
作者
Aukrust, P
Hestdal, K
Lien, E
Bjerkeli, V
Nordoy, I
Espevik, T
Muller, F
Froland, SS
机构
[1] UNIV OSLO, NATL HOSP,RIKSHOSP,SECT CLIN IMMUNOL & INFECT DIS, MED DEPT A, OSLO, NORWAY
[2] UNIV OSLO, NATL HOSP, RIKSHOSP, INTERNAL MED RES INST, OSLO, NORWAY
[3] UNIV OSLO, NATL HOSP, RIKSHOSP, DEPT PEDIAT RES, OSLO, NORWAY
[4] NORWEGIAN UNIV SCI & TECHNOL, INST CANC RES & MOL BIOL, N-7034 TRONDHEIM, NORWAY
关键词
D O I
10.1086/516510
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 effect of a single bolus injection (0.4 g/kg) of intravenous immunoglobulin (IVIG) on the tumor necrosis factor (TNF) system in human immunodeficiency virus type 1 (HIV-1)-infected patients was investigated. At 140 h after infusion, there was a significant decrease in levels of TNF-alpha and a significant increase in levels of soluble TNF receptors (sTNFR) in both plasma and lipopolysaccharide-stimulated peripheral blood mononuclear cells (PBMC). A rapid (within 1 h) decline in expression of membrane-bound TNF-alpha and p55-TNFR on PBMC persisted throughout the study, In contrast, there was an increased expression of membrane-bound p75-TNFR after 140 h. IVIG administration also resulted in significantly increased numbers of circulating CD4 lymphocytes, correlated with down-regulation of TNF-alpha activity in PBMC supernatants. Thus, down-regulation of the abnormally increased TNF-alpha activity may be achieved by IVIG administration. Studies evaluating the possible therapeutic role of long-term TNF-alpha suppression by IVIG may be warranted in HIV-1-infected patients.
引用
收藏
页码:913 / 923
页数:11
相关论文
共 61 条
  • [1] INTRAVENOUS IMMUNOGLOBULIN TREATMENT OF EXPERIMENTAL T-CELL-MEDIATED AUTOIMMUNE-DISEASE - UP-REGULATION OF T-CELL PROLIFERATION AND DOWN-REGULATION OF TUMOR-NECROSIS-FACTOR-ALPHA SECRETION
    ACHIRON, A
    MARGALIT, R
    HERSHKOVIZ, R
    MARKOVITS, D
    RESHEF, T
    MELAMED, E
    COHEN, IR
    LIDER, O
    [J]. JOURNAL OF CLINICAL INVESTIGATION, 1994, 93 (02) : 600 - 605
  • [2] STABILIZATION OF THE BIOACTIVITY OF TUMOR-NECROSIS-FACTOR BY ITS SOLUBLE RECEPTORS
    ADERKA, D
    ENGELMANN, H
    MAOR, Y
    BRAKEBUSCH, C
    WALLACH, D
    [J]. JOURNAL OF EXPERIMENTAL MEDICINE, 1992, 175 (02) : 323 - 329
  • [3] AGOSTINI C, 1995, J IMMUNOL, V154, P2928
  • [4] ANDERSSON JP, 1990, IMMUNOLOGY, V71, P372
  • [5] [Anonymous], 1992, MMWR-MORBID MORTAL W, V41, P1
  • [6] INHIBITION OF THE PRODUCTION AND EFFECTS OF INTERLEUKIN-1 AND TUMOR-NECROSIS-FACTOR-ALPHA IN RHEUMATOID-ARTHRITIS
    AREND, WP
    DAYER, JM
    [J]. ARTHRITIS AND RHEUMATISM, 1995, 38 (02): : 151 - 160
  • [7] AUKRUST P, 1994, BLOOD, V84, P2136
  • [8] Persistent activation of the tumor necrosis factor system in a subgroup of patients with common variable immunodeficiency-possible immunologic and clinical consequences
    Aukrust, P
    Lien, E
    Kristoffersen, AK
    Muller, F
    Haug, CJ
    Espevik, T
    Froland, SS
    [J]. BLOOD, 1996, 87 (02) : 674 - 681
  • [9] Modulation of lymphocyte and monocyte activity after intravenous immunoglobulin administration in vivo
    Aukrust, P
    Muller, F
    Nordoy, I
    Haug, CJ
    Froland, SS
    [J]. CLINICAL AND EXPERIMENTAL IMMUNOLOGY, 1997, 107 (01) : 50 - 56
  • [10] SERUM LEVELS OF TUMOR-NECROSIS-FACTOR-ALPHA (TNF-ALPHA) AND SOLUBLE TNF RECEPTORS IN HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 INFECTION - CORRELATIONS TO CLINICAL, IMMUNOLOGICAL, AND VIROLOGICAL PARAMETERS
    AUKRUST, P
    LIABAKK, NB
    MULLER, F
    LIEN, E
    ESPEVIK, T
    FROLAND, SS
    [J]. JOURNAL OF INFECTIOUS DISEASES, 1994, 169 (02) : 420 - 424