PMID- 10089914
OWN - NLM
STAT- MEDLINE
DCOM- 19990421
LR  - 20191024
IS  - 0301-472X (Print)
IS  - 0301-472X (Linking)
VI  - 27
IP  - 3
DP  - 1999 Mar
TI  - Interferon-gamma rescues TNF-alpha-induced apoptosis mediated by up-regulation of 
      TNFR2 on EoL-1 cells.
PG  - 512-9
AB  - Recent studies show that apoptosis is important for the resolution of chronic 
      inflammation. Using a human myeloblastic leukemia cell line, EoL-1, we 
      investigated the effect of interferon-gamma (IFN-gamma), which differentiates 
      EoL-1 into monocyte/macrophage-like cells on Fas antigen (Fas)- and tumor 
      necrosis factor-alpha (TNF alpha)-induced apoptosis. Both TNF and anti-Fas 
      monoclonal antibody (CH-11) induced apoptosis of EoL-1 cells. Pretreatment with 
      IFN-gamma for 72 hours enhanced the CH-11-induced apoptosis with up-regulation of 
      Fas. However, the treatment markedly inhibited the TNF-induced apoptosis. In flow 
      cytometric analysis, EoL-1 expressed two types of tumor necrosis factor receptors 
      (TNFR1 and TNFR2), and the expression of TNFR2 but not of TNFR1 was up-regulated 
      significantly after the IFN-gamma treatment. The TNF-induced apoptosis was 
      mimicked by a TNFR1 stimulating antibody (htr-9), and was reversed by a TNFR1 
      blocking antibody (H398). Although the TNFR1-mediated cytotoxic signal was not 
      affected by IFN-gamma pretreatment, blocking TNFR2 by a specific antagonistic 
      antibody (utr-1) canceled the inhibitory effect of IFN-gamma. In conclusion, 
      TNF-induced apoptosis was mediated preferentially by TNFR1, and the 
      anti-apoptotic effect of IFN-gamma was result from up-regulated TNFR2 in EoL-1 
      cell line. This cell line is a useful model to provide new insights into 
      crosstalk among Fas/FasL-, TNF-, and IFN-gamma-mediated signaling.
FAU - Horie, T
AU  - Horie T
AD  - First Department of Internal Medicine, Gunma University Faculty of Medicine, 
      Japan.
FAU - Dobashi, K
AU  - Dobashi K
FAU - Iizuka, K
AU  - Iizuka K
FAU - Yoshii, A
AU  - Yoshii A
FAU - Shimizu, Y
AU  - Shimizu Y
FAU - Nakazawa, T
AU  - Nakazawa T
FAU - Mori, M
AU  - Mori M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Exp Hematol
JT  - Experimental hematology
JID - 0402313
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antigens, CD)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type II)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (fas Receptor)
RN  - 82115-62-6 (Interferon-gamma)
SB  - IM
MH  - Antibodies, Monoclonal/pharmacology
MH  - Antigens, CD/biosynthesis/drug effects/genetics/immunology/*physiology
MH  - Apoptosis/*drug effects/physiology
MH  - Cell Differentiation/drug effects
MH  - Humans
MH  - Interferon-gamma/*pharmacology
MH  - Leukemia, Myeloid, Acute/pathology
MH  - Neoplasm Proteins/antagonists & inhibitors/physiology
MH  - Receptors, Tumor Necrosis Factor/biosynthesis/drug 
      effects/genetics/immunology/*physiology
MH  - Receptors, Tumor Necrosis Factor, Type I
MH  - Receptors, Tumor Necrosis Factor, Type II
MH  - Recombinant Proteins
MH  - Tumor Cells, Cultured
MH  - Tumor Necrosis Factor-alpha/*antagonists & inhibitors/pharmacology
MH  - Up-Regulation
MH  - fas Receptor/immunology/physiology
EDAT- 1999/03/25 00:00
MHDA- 1999/03/25 00:01
CRDT- 1999/03/25 00:00
PHST- 1999/03/25 00:00 [pubmed]
PHST- 1999/03/25 00:01 [medline]
PHST- 1999/03/25 00:00 [entrez]
AID - S0301-472X(98)00058-7 [pii]
AID - 10.1016/s0301-472x(98)00058-7 [doi]
PST - ppublish
SO  - Exp Hematol. 1999 Mar;27(3):512-9. doi: 10.1016/s0301-472x(98)00058-7.