PMID- 9746065
OWN - NLM
STAT- MEDLINE
DCOM- 19981208
LR  - 20190831
IS  - 0146-6615 (Print)
IS  - 0146-6615 (Linking)
VI  - 56
IP  - 2
DP  - 1998 Oct
TI  - Interleukin 12 enhances deficient HCV-antigen-induced Th1-type immune response of 
      peripheral blood mononuclear cells.
PG  - 112-7
AB  - The aim of this study was to examine the possible immunomodulating effects of 
      rhIL-12 on the immune response induced by different hepatitis C virus (HCV) 
      antigens. Freshly isolated peripheral blood mononuclear cells (PBMC) of 33 
      patients with chronic HCV infection were stimulated with optimal concentrations 
      of antigens from the NS3, NS4, NS5, and core region of HCV in the absence or 
      presence of interleukin-12 (IL-12). Stimulation by alpha-CD3 + alpha-CD28, 
      lipopolysaccharide (LPS), and pokeweed mitogen (PWM) were used as controls. 
      Proliferation and cytokine production were determined by 3H-thymidine uptake and 
      enzyme-linked immunosorbent assay (ELISA) after 72 hr. After stimulation with 
      antigen or antigen + IL-12, increased proliferation and production of 
      interferon-gamma (IFN gamma) and tumor necrosis factor-alpha (TNF alpha) were 
      observed in 23 of the 33 patients. Thus, a separation of the patients into 
      HCV-antigen/IL-12 responders (group 1, n = 23) and HCV-antigen/IL-12 
      nonresponders (group 2, n = 10) was possible. Lower baseline IL-12- and 
      LPS-induced IFN gamma, TNF alpha, and IL-12 production was observed in group 2 
      due to a possible dysfunction of accessory cells. Significant antigen-induced 
      Th2-type cytokine (IL-4, IL-10, IL-13) production was not found. According to 
      clinical and serological parameters, group 2 comprised mostly patients with 
      advanced liver disease. These data suggest an HCV-related cellular immune defect 
      in patients with hepatitis C that can be restored in most patients by IL-12.
FAU - Schlaak, J F
AU  - Schlaak JF
AD  - First Department of Medicine, University of Mainz, Germany.
FAU - Pitz, T
AU  - Pitz T
FAU - Lohr, H F
AU  - Lohr HF
FAU - Meyer zum Buschenfelde, K H
AU  - Meyer zum Buschenfelde KH
FAU - Gerken, G
AU  - Gerken G
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Med Virol
JT  - Journal of medical virology
JID - 7705876
RN  - 0 (Cytokines)
RN  - 0 (Hepatitis C Antigens)
RN  - 0 (RNA, Viral)
RN  - 187348-17-0 (Interleukin-12)
SB  - IM
MH  - Cytokines/biosynthesis
MH  - Hepacivirus/*immunology/physiology
MH  - Hepatitis C/*immunology/physiopathology
MH  - Hepatitis C Antigens/*immunology
MH  - Humans
MH  - Interleukin-12/*immunology
MH  - Leukocytes, Mononuclear/*immunology
MH  - Lymphocyte Activation
MH  - RNA, Viral/analysis
MH  - Th1 Cells/*immunology
EDAT- 1998/09/24 02:03
MHDA- 2000/06/20 09:00
CRDT- 1998/09/24 02:03
PHST- 1998/09/24 02:03 [pubmed]
PHST- 2000/06/20 09:00 [medline]
PHST- 1998/09/24 02:03 [entrez]
AID - 10.1002/(SICI)1096-9071(199810)56:2<112::AID-JMV2>3.0.CO;2-B [pii]
AID - 10.1002/(sici)1096-9071(199810)56:2<112::aid-jmv2>3.0.co;2-b [doi]
PST - ppublish
SO  - J Med Virol. 1998 Oct;56(2):112-7. doi: 
      10.1002/(sici)1096-9071(199810)56:2<112::aid-jmv2>3.0.co;2-b.