Human dermal microvascular endothelial cells behave like umbilical vein endothelial cells in T-cell adhesion studies

J Invest Dermatol. 1987 Mar;88(3):340-4. doi: 10.1111/1523-1747.ep12466229.


The adhesion of T lymphocytes to human dermal microvascular endothelial cells (DMVEC) in vitro has been tested after stimulation of the DMVEC with gamma interferon (IFN-gamma), interleukin 1 (IL-1), or a bacterial lipopolysaccharide (LPS). These agents enhanced T-cell adhesion in a manner similar to that previously observed with human umbilical vein endothelial cells (UVEC). Moreover, phorbol ester stimulation of T cells enhanced T-cell adhesion to both DMVEC and UVEC. Unstimulated and phorbol ester-enhanced T-cell adhesion to both DMVEC and UVEC was strongly inhibited by monoclonal antibody (Mab) 60.3 against the surface membrane CDw18 glycoprotein complex. In contrast, Mab 60.3 had a much weaker inhibitory effect on the binding enhancement due to IL-1, LPS, or IFN-gamma, suggesting that these agents may enhance adhesion by a mechanism at least partially independent of CDw18. These observations suggest that DMVEC behave in a similar fashion to UVEC in T-cell adhesion studies, and support previous conclusions that modulation of lymphocyte endothelial cell adhesion by cytokines, bacterial products, and phorbol esters may be relevant to lymphocyte adhesion and migration in vivo.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Antibodies, Monoclonal / physiology
  • Capillaries / cytology
  • Capillaries / physiology
  • Cell Adhesion / drug effects
  • Endothelium / cytology
  • Endothelium / physiology
  • Humans
  • Interferon-gamma / pharmacology
  • Interleukin-1 / pharmacology
  • Phorbol Esters / pharmacology
  • Skin / blood supply*
  • T-Lymphocytes / physiology*
  • Umbilical Veins / cytology
  • Umbilical Veins / physiology


  • Antibodies, Monoclonal
  • Interleukin-1
  • Phorbol Esters
  • Interferon-gamma