Format

Send to

Choose Destination
See comment in PubMed Commons below
Eur J Cell Biol. 1993 Aug;61(2):290-8.

VCAM-1 is not involved in LPAM-1 (alpha 4 beta p/alpha 4 beta 7) mediated binding of lymphoma cells to high endothelial venules of mucosa-associated lymph nodes.

Author information

1
Hans Spemann Laboratory, Max Planck Institute for Immunobiology, Freiburg/Germany.

Abstract

The migration of lymphocytes from the blood into various lymphoid organs (lymphocyte homing) occurs in specialized high endothelial venules (HEV). Homing of lymphocytes into mucosa-associated lymph nodes in the mouse is mediated at least in part by the lymphocyte homing receptor LPAM-1, an integrin which has been identified as the heterodimer alpha 4 beta p (alpha 4 beta 7 in humans). The HEV-ligand for this integrin in the homing process has not yet been identified. VCAM-1, a cytokine-inducible, endothelial adhesion molecule for lymphocytes and monocytes, was recently demonstrated in vitro to be a ligand for the alpha 4 beta p integrin. We have tested whether VCAM-1 could be a candidate for an alpha 4 beta p ligand on HEV. Two findings strongly argue against this possibility: First, an anti-VCAM-1 monoclonal antibody (mAb) failed to block the binding of the mouse T-lymphoma TK-1 to HEV in cryostat sections of mesenteric lymph nodes, even though this antibody blocked alpha 4 beta p mediated binding of TK-1 cells to VCAM-1 on TNF-alpha-activated mouse endothelioma cells. Second, expression of VCAM-1 on lymph node endothelium was undetectably low as tested by immunofluorescence staining of mouse tissue sections using four different mAbs against mouse VCAM-1, three of which are described in this report. Surprisingly, expression of VCAM-1 on lymph node endothelium was not found even in mice which had been treated systemically with high doses of TNF-alpha or LPS, although VCAM-1 expression was strongly induced on endothelial of all other organs that were analyzed.(ABSTRACT TRUNCATED AT 250 WORDS)

PMID:
7693472
[Indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Loading ...
    Support Center