PMID- 7738362
OWN - NLM
STAT- MEDLINE
DCOM- 19950602
LR  - 20190723
IS  - 0022-202X (Print)
IS  - 0022-202X (Linking)
VI  - 104
IP  - 5
DP  - 1995 May
TI  - Pentoxifylline inhibits tumor necrosis factor-alpha (TNF alpha)-induced 
      T-lymphoma cell adhesion to endothelioma cells.
PG  - 824-8
AB  - Pentoxifylline, a methylxanthine derivative, has been shown to inhibit 
      T-cell-mediated cutaneous immune response by yet ill-understood mechanisms. 
      Because cell adhesion to endothelial cells is a critical step in the initiation 
      of such immune responses, we analyzed whether pentoxifylline would affect this 
      process. To address this issue, adhesion of mouse T-lymphoma cells (TK-1) to 
      mouse endothelioma cells (eEnd.2), either untreated or stimulated with tumor 
      necrosis factor-alpha (TNF alpha), was studied. Pentoxifylline reduced the 
      ability of endothelioma cells stimulated with different concentrations of TNF 
      alpha, but not of untreated endothelioma cells, to bind T-lymphoma cells in 
      dose-dependent (10(-5)-10(-3) M) fashion. Selective incubation of either 
      endothelioma cells or T-lymphoma cells revealed that pentoxifylline acted 
      exclusively on the endothelioma cells, even when added after TNF alpha 
      stimulation. We questioned whether pentoxifylline suppressed T-lymphoma 
      cell/endothelioma cell interactions by interfering with adhesion molecules 
      expressed by either cell. However, as determined by flow cytometry, 
      pentoxifylline did not alter TNF alpha-induced upregulation of intercellular 
      adhesion molecule-1 or vascular cellular adhesion molecule-1 on endothelioma 
      cells nor did it affect constitutive CD11a, CD18, or alpha 4-integrin expression 
      on T-lymphoma cells, suggesting that rather than affecting quantitative 
      expression of these adhesion molecules, pentoxifylline might modulate their 
      avidity. We conclude that pentoxifylline in therapeutically achievable 
      concentrations is a potent inhibitor of TNF alpha-induced T-lymphoma cell 
      adhesion to endothelioma cells. This finding may account, at least in part, for 
      the recently discovered anti-inflammatory action of pentoxifylline.
FAU - Weiss, J M
AU  - Weiss JM
AD  - Department of Dermatology, University of Freiburg, Germany.
FAU - Vanscheidt, W
AU  - Vanscheidt W
FAU - Pilarski, K A
AU  - Pilarski KA
FAU - Weyl, A
AU  - Weyl A
FAU - Peschen, M
AU  - Peschen M
FAU - Schopf, E
AU  - Schopf E
FAU - Vestweber, D
AU  - Vestweber D
FAU - Simon, J C
AU  - Simon JC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Invest Dermatol
JT  - The Journal of investigative dermatology
JID - 0426720
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - SD6QCT3TSU (Pentoxifylline)
SB  - IM
MH  - Animals
MH  - Cell Adhesion/drug effects
MH  - Cell Line
MH  - Lymphangioma/drug therapy/*pathology
MH  - Lymphoma, T-Cell, Cutaneous/drug therapy/*pathology
MH  - Mice
MH  - Pentoxifylline/*pharmacology
MH  - Rats
MH  - Skin Neoplasms/drug therapy/pathology
MH  - Tumor Cells, Cultured
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1995/05/01 00:00
MHDA- 1995/05/01 00:01
CRDT- 1995/05/01 00:00
PHST- 1995/05/01 00:00 [pubmed]
PHST- 1995/05/01 00:01 [medline]
PHST- 1995/05/01 00:00 [entrez]
AID - S0022-202X(15)42137-2 [pii]
AID - 10.1111/1523-1747.ep12607010 [doi]
PST - ppublish
SO  - J Invest Dermatol. 1995 May;104(5):824-8. doi: 10.1111/1523-1747.ep12607010.