International Immunology, Vol 9, 147-159, Copyright © 1997 by Oxford University Press
U Tschoetschel, J Schwing, S Frosch, E Schmitt, D Schuppan and AB Reske-Kunz
In this study we investigated the co-stimulatory signaling capacity of
diverse proteins of the extracellular matrix (ECM) for murine resting CD4+
T cells and Th1 clone cells, activated by immobilized anti-CD3 mAb. ECM
proteins used in various concentrations had no effect on IL-2 production or
proliferation of highly purified CD4+ T cell populations. When the
preparation of CD4+ T cells contained contaminating accessory cells, IL-2
secretion and proliferation was enhanced in the presence of co-immobilized
collagens or fibronectin. However, the level of proliferation attainable by
added irradiated splenocytes was not reached. Using Th1 cell clone M4,
enhanced production of IL-2 in the presence of immobilized ECM proteins was
observed. At a submitogenic anti-CD3 mAb dose, proliferation of M4 T cells
was augmented by the ECM proteins in a concentration range that optimally
induced IL-2 production. IL-2R p55 was up-regulated on M4 T cells by
collagen type IV and fibronectin to the same level that was induced by
exogenously added IL-2, whereas added accessory cells induced a higher
level of IL- 2R p55 expression. Likewise, in dot-blot analysis a comparable
quantity of IL-2R p55- and p75-specific transcripts was induced by collagen
type IV or fibronectin and by IL-2, which was lower than that induced by
antigen-presenting cells. Our data suggest that the enhanced proliferation
of M4 T cells induced by ECM proteins is not the consequence of direct
up-regulation of IL-2R, but appears to be due indirectly to elevated
secretion of IL-2. At an optimal anti-CD3 mAb dose the collagens inhibited
M4 T cell proliferation. Diminished cell surface expression of IL-2R p55
following stimulation with anti-CD3 mAb plus collagen type IV compared with
anti-CD3 mAb alone was observed and may be responsible for growth
inhibition.
ARTICLES
Modulation of proliferation and lymphokine secretion of murine CD4+ T cells and cloned Th1 cells by proteins of the extracellular matrix
Department of Dermatology, Johannes Gutenberg-University, Mainz, Germany.
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