PMID- 8818539
OWN - NLM
STAT- MEDLINE
DCOM- 19961218
LR  - 20061115
IS  - 1043-4666 (Print)
IS  - 1043-4666 (Linking)
VI  - 8
IP  - 6
DP  - 1996 Jun
TI  - The role of the two TNF receptors in proliferation, NF-kappa B activation and 
      discrimination between TNF and LT alpha signalling in the human myeloma cell line 
      OH-2.
PG  - 430-8
AB  - We wanted to study the role of the two TNF receptors (TNFR) in mediating 
      proliferation and nuclear transcription factor kappa-B (NF-kappa B) activation in 
      the human myeloma cell line OH-2. Agonistic antibodies to either of the TNFRs 
      were able to induce proliferation in OH-2 cells, while only antibodies to the p55 
      TNFR could activate the NF-kappa B. TNF was 100-1000-fold more potent than LT 
      alpha in activation of NF-kappa B and in induction of proliferation in OH-2 
      cells. Only a 2-fold difference between TNF and LT alpha in affinity for the 
      TNFRs was detected, indicating that the difference in the specific activities of 
      the cytokines can not be explained by different binding affinities. Antagonistic 
      mAbs to either the p55 or p75 TNFR blocked the binding of both cytokines to the 
      cells and significantly inhibited proliferation induced by TNF. On the other 
      hand, only the p55 TNFR mAb was capable of inhibiting the proliferative effect of 
      LT alpha. The p55 mAb 44E potentiated the proliferation induced by LT alpha, but 
      did not affect the TNF-mediated proliferation. The data lead to the following 
      conclusions: (1) both TNFR species trigger proliferation of OH-2 cells, whereas 
      only the p55 TNFR activates the NF-kappa B; (2) TNF signals through both TNFR, 
      whereas LT alpha mediates its signal through the p55 TNFR only; (3) activation of 
      the p55 TNFR by LT alpha is not optimal, but can be facilitated by co-stimulating 
      the receptor with the mAb 44E.
FAU - Borset, M
AU  - Borset M
AD  - Institute of Cancer Research and Molecular Biology, University Medical Center, 
      University of Trondheim, Norway. magne.borset@ifk.unit.no
FAU - Medvedev, A E
AU  - Medvedev AE
FAU - Sundan, A
AU  - Sundan A
FAU - Espevik, T
AU  - Espevik T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Cytokine
JT  - Cytokine
JID - 9005353
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antigens, CD)
RN  - 0 (Lymphotoxin-alpha)
RN  - 0 (NF-kappa B)
RN  - 0 (Receptors, Tumor Necrosis Factor)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type II)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Antibodies, Monoclonal
MH  - Antigens, CD/*physiology
MH  - Cell Division
MH  - Electrophoresis, Polyacrylamide Gel
MH  - Humans
MH  - Lymphotoxin-alpha/*physiology
MH  - Multiple Myeloma/*metabolism
MH  - NF-kappa B/*metabolism
MH  - Receptors, Tumor Necrosis Factor/*physiology
MH  - Receptors, Tumor Necrosis Factor, Type I
MH  - Receptors, Tumor Necrosis Factor, Type II
MH  - *Signal Transduction
MH  - Tumor Cells, Cultured
MH  - Tumor Necrosis Factor-alpha/*physiology
EDAT- 1996/06/01 00:00
MHDA- 1996/06/01 00:01
CRDT- 1996/06/01 00:00
PHST- 1996/06/01 00:00 [pubmed]
PHST- 1996/06/01 00:01 [medline]
PHST- 1996/06/01 00:00 [entrez]
AID - S1043-4666(96)90059-9 [pii]
AID - 10.1006/cyto.1996.0059 [doi]
PST - ppublish
SO  - Cytokine. 1996 Jun;8(6):430-8. doi: 10.1006/cyto.1996.0059.