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Specific down-regulation of proliferative T cell alloresponsiveness by interference with CD2/LFA-3 and LFA-1/ICAM-1 in vitro.

G A Böhmig, J Kovarik, W Holter, E Pohanka and G J Zlabinger
J Immunol April 15, 1994, 152 (8) 3720-3728;
G A Böhmig
Institute of Immunology, University of Vienna, Austria.
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J Kovarik
Institute of Immunology, University of Vienna, Austria.
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W Holter
Institute of Immunology, University of Vienna, Austria.
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E Pohanka
Institute of Immunology, University of Vienna, Austria.
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G J Zlabinger
Institute of Immunology, University of Vienna, Austria.
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Abstract

T cell activation requires Ag contact with the TCR in the presence of costimulatory signals provided by APCs. When Ag is presented without costimulation, T cells are functionally inactivated. Here we demonstrate that interference with distinct adhesion molecules during Ag contact using mAbs leads to Ag-specific functional inactivation of alloreactive T cells. We found that the presence of a mixture of mAbs specific for CD2, LFA-3, LFA-1 alpha- and beta-chain, and ICAM-1 during primary MLC leads to down-regulation of secondary proliferative responses to Ag from the donor used for priming. Cells from pretreated cultures proliferated well, however, when stimulated with Ag from third party donors, mitogens, or mitogenic CD3 mAb. Because specific reactivity could be restored by addition of IL-2 to restimulation cultures, altered secondary responsiveness appeared to be caused by anergy and not by elimination of specific clones. Furthermore, specific down-regulation of alloresponsiveness was prevented by addition of IL-2 to primary cultures in the presence of mAb. Interference by mAb with either CD2/LFA-3, LFA-1/ICAM-1, CD2/LFA-1, or LFA-3/ICAM-1 had a substantial, though less pronounced effect on secondary responsiveness. After pretreatment with the Ab mixture, CTL generation was substantially but incompletely down-regulated against the original and third party donors. Because a decrease in the reactivity of unstimulated responders by culture was also observed, these findings might be explained by the loss of cytotoxic precursors after culturing under nonstimulating conditions. In conclusion, our data demonstrate that T cells enter a state of anergy when T cell activation is modulated by simultaneous interference with distinct adhesion molecules during Ag contact, which thus might reflect at least partly overlapping functions of particular receptor-ligand pairs in T cell costimulation.

  • Copyright © 1994 by American Association of Immunologists

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The Journal of Immunology
Vol. 152, Issue 8
15 Apr 1994
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Specific down-regulation of proliferative T cell alloresponsiveness by interference with CD2/LFA-3 and LFA-1/ICAM-1 in vitro.
G A Böhmig, J Kovarik, W Holter, E Pohanka, G J Zlabinger
The Journal of Immunology April 15, 1994, 152 (8) 3720-3728;

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Specific down-regulation of proliferative T cell alloresponsiveness by interference with CD2/LFA-3 and LFA-1/ICAM-1 in vitro.
G A Böhmig, J Kovarik, W Holter, E Pohanka, G J Zlabinger
The Journal of Immunology April 15, 1994, 152 (8) 3720-3728;
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Print ISSN 0022-1767        Online ISSN 1550-6606