AJP - Lung Cellular and Molecular Physiology, Vol 267, Issue 5 543-L550, Copyright © 1994 by American Physiological Society
Expression of activation markers by human lung T cells after adherence to lung epithelial cells
B. Bruinier, F. H. Krouwels, B. E. Hol, H. M. Jansen, T. A. Out and R. Lutter
Department of Pulmonology, University of Amsterdam, The Netherlands.
Both increased T cell numbers and their increased activation state have
implicated an important role for T cells in chronic inflammatory reactions
seen in the airways of (allergic) asthmatics. Airway epithelial cells are
frequently exposed to stimuli that cause the release of mediators and the
expression of cell adhesion molecules. We have examined whether human
airway epithelial cells can activate lung-derived T cells. Clonal lung T
cells showed an increased adherence to transformed airway epithelial cells
that had been exposed previously for 2 h to human recombinant
interferon-gamma (IFN-gamma; 100 U/ml). After an additional 16-24 h of
culturing in the absence or presence of epithelial cells, T cells expressed
increased levels of both the alpha-chain of the interleukin-2 receptor
(IL-2R, CD25) and the transferrin receptor (CD71), both markers of T cell
activation. T cells apparently activated by epithelial cells, however, did
not produce IFN-gamma or IL-4 nor showed an increased proliferation on the
addition of IL-2 (5-50 U/ml). The induced adherence to and the activation
of T cells by epithelial cells is mediated largely by CD2 and its ligand
lymphocyte functional antigen-3, a pathway known to up- and downregulate T
cell functions.
