PMID- 8760279
OWN - NLM
STAT- MEDLINE
DCOM- 19960924
LR  - 20190826
IS  - 0161-5890 (Print)
IS  - 0161-5890 (Linking)
VI  - 33
IP  - 7-8
DP  - 1996 May-Jun
TI  - Tumor necrosis factor-alpha (TNF-alpha) induces a reversible, time- and 
      dose-dependent adhesion of progenitor T cells to endothelial cells.
PG  - 671-80
AB  - Recent in vivo studies suggest that tumor necrosis factor-alpha (TNF-alpha) is 
      involved in the development of the thymus. We postulated that this inflammatory 
      mediator could regulate the influx of progenitor T cells into the thymus. Using 
      an in vitro static adhesion system, we found that TNF-alpha increases the 
      adhesion of a murine progenitor T cell line (FTF1) to a bovine aortic endothelial 
      cell line (1F8), human umbilical vein endothelial (HUVE) cells, and a murine 
      arterial endothelial (MAE) cell line. TNF-alpha treatment of the 1F8 cells 
      resulted in a time- and dose-dependent increase in the adherence of FTF1 cells. 
      Adherence increased during the first 6 hr of treatment with TNF-alpha 
      concentrations ranging from 10(-11) to 10(-9) M. Maximal adherence (6 hr 
      treatment with 10(-10) M of TNF-alpha) was approximately 4.5-fold larger than 
      that of untreated monolayers. A slow decrease in adherence, down to approximately 
      2-fold at 48 hr, was observed beyond 12 hr of TNF-alpha treatment; in contrast, 
      removal of TNF-alpha after 6 hr of continued stimulation caused the adherence to 
      return to pre-stimulation levels within 24-30 hr. Adhesion of FTF1 cells to 
      TNF-alpha treated 1F8 cells was almost completely blocked by a monoclonal 
      antibody against murine CD49d (very late antigen-4) expressed on FTF1 cells. 
      TNF-alpha-induced adhesion of FTF1 cells to MAE cells was also blocked by 
      monoclonal antibodies against murine CD49d and CD106 (vascular cell adhesion 
      molecule-1). These results support the notion that local secretion of TNF-alpha 
      could modulate the dynamics of adhesion of progenitor T cells to the thymic 
      endothelium.
FAU - Aparicio, C L
AU  - Aparicio CL
AD  - Department of Chemical and Biochemical Engineering, Rutgers University, 
      Piscataway, NJ 08855, USA.
FAU - Berthiaume, F
AU  - Berthiaume F
FAU - Chang, C C
AU  - Chang CC
FAU - Yarmush, M L
AU  - Yarmush ML
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Mol Immunol
JT  - Molecular immunology
JID - 7905289
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Animals
MH  - Antibodies, Monoclonal/pharmacology
MH  - Binding, Competitive/immunology
MH  - Cattle
MH  - Cell Adhesion/drug effects/immunology
MH  - Cell Line
MH  - Dose-Response Relationship, Immunologic
MH  - Endothelium, Vascular/cytology/*drug effects/immunology
MH  - Hematopoietic Stem Cells/*drug effects/immunology
MH  - Humans
MH  - Kinetics
MH  - Mice
MH  - T-Lymphocytes/*drug effects/physiology
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1996/05/01 00:00
MHDA- 1996/05/01 00:01
CRDT- 1996/05/01 00:00
PHST- 1996/05/01 00:00 [pubmed]
PHST- 1996/05/01 00:01 [medline]
PHST- 1996/05/01 00:00 [entrez]
AID - 10.1016/0161-5890(96)00013-2 [doi]
PST - ppublish
SO  - Mol Immunol. 1996 May-Jun;33(7-8):671-80. doi: 10.1016/0161-5890(96)00013-2.