PMID- 9162265
OWN - NLM
STAT- MEDLINE
DCOM- 19970529
LR  - 20060719
IS  - 1018-8916 (Print)
IS  - 1018-8916 (Linking)
VI  - 15
IP  - 2-3
DP  - 1996-1997
TI  - Adhesion of activated natural killer cells to tumor necrosis factor-alpha-treated 
      endothelium under physiological flow conditions.
PG  - 154-63
AB  - Adhesion of activated natural killer (A-NK) cells to activated and nonactivated 
      endothelial cells in vitro was studied under dynamic flow conditions. Endothelial 
      cells grown on glass slides were either treated with tumor necrosis factor-alpha 
      (TNF alpha) or medium, then placed into a flow chamber over which suspensions of 
      A-NK cells were passed using a range of defined shear stress levels. Significant 
      numbers of binding cells could be consistently observed at shear stress levels 
      less than 3 dyn/cm2 on TNF alpha-activated endothelium or at 0.59 dyn/cm2 on 
      nonactivated endothelium. Stable adhesion occurred rapidly following the initial 
      interaction of the following cells with the endothelium in the absence of 
      detectable rolling. Pretreatment of the A-NK cells with monoclonal antibodies 
      directed against CD18 (LFA-1) or CD49d (VLA-4) resulted in a significant 
      reduction in the number of binding cells. Simultaneous treatment with both 
      monoclonal antibodies eliminated all A-NK adhesion occurring over 0.5 dyn/cm2. 
      Pretreatment of the endothelial cells with antibodies against E- or P-selectin 
      resulted in a small but significant reduction in binding only at 0.5 dyn/cm2. The 
      binding efficiency of the A-NK cells was similar to that previously observed for 
      T lymphocytes under the same conditions. Once bound, approximately half of the 
      adherent cells could resist detachment when exposed to wall shear stresses over 
      12 dyn/cm2. These findings indicate that A-NK cell adhesion to activated 
      endothelium can occur under shear stress conditions which are representative of 
      postcapillary venules and that this binding is mediated principally by both CD18 
      and CD49d. A-NK cell adhesion also occurs to nonactivated endothelium but only at 
      wall shear stress levels less than 1 dyn/cm2.
FAU - Melder, R J
AU  - Melder RJ
AD  - Edwin L. Steele Laboratory, Department of Radiation Oncology, Massachusetts 
      General Hospital, Boston 02114, USA.
FAU - Koenig, G C
AU  - Koenig GC
FAU - Munn, L L
AU  - Munn LL
FAU - Jain, R K
AU  - Jain RK
LA  - eng
PT  - Journal Article
PL  - Switzerland
TA  - Nat Immun
JT  - Natural immunity
JID - 9206126
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Cell Adhesion/immunology
MH  - Cells, Cultured
MH  - Endothelium, Vascular/drug effects/*immunology/physiology
MH  - Humans
MH  - Killer Cells, Natural/drug effects/*immunology/physiology
MH  - Lymphocyte Activation
MH  - Rheology
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1996/01/01 00:00
MHDA- 1996/01/01 00:01
CRDT- 1996/01/01 00:00
PHST- 1996/01/01 00:00 [pubmed]
PHST- 1996/01/01 00:01 [medline]
PHST- 1996/01/01 00:00 [entrez]
PST - ppublish
SO  - Nat Immun. 1996-1997;15(2-3):154-63.