The JI
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     
 

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lorre, K.
Right arrow Articles by Ceuppens, J. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lorre, K.
Right arrow Articles by Ceuppens, J. L.

The Journal of Immunology, Vol 144, Issue 12 4681-4687, Copyright © 1990 by American Association of Immunologists

ARTICLES

IL-6 is an accessory signal in the alternative CD2-mediated pathway of T cell activation

K Lorre, J Van Damme, J Verwilghen, ML Baroja and JL Ceuppens
Department of Medicine and Pathophysiology, University of Leuven, Belgium.

Recent studies have demonstrated that IL-1 and IL-6 are synergistic accessory signals for activation of T cells. In this study, highly purified human T cells were cultured with either a stimulating pair of anti-CD2 mAb or with immobilized anti-CD3 mAb. Monocytes, a cellfree monocyte culture supernatant or IL-1 were required for anti-CD2- stimulated T cell proliferation, and they each strongly enhanced anti- CD3-induced T cell growth. IL-6 was synergistic with IL-1 as a helper factor for T cell growth after activation via CD2, but we could not demonstrate any effect of IL-6 in the CD3 pathway. The mechanism of the synergistic helper activity of IL-1 and IL-6 on T cell activation in the CD2 pathway was further examined. IL-1 (but not IL-6) was required for induction of IL-2 production. Both IL-1 and IL-6 enhanced IL-2R (p55) expression and the proliferative response to IL-2. T cell proliferation after stimulation with anti-CD2 and IL-1 or IL-1/IL-6 proceeded through an autocrine IL-2-dependent pathway. Moreover we found that, in the absence of IL-1, IL-6 still supported a transient and limited proliferation of anti-CD2- (but not of anti-CD3-) stimulated T cells, which apparently was independent of the autocrine growth factors IL-2 or IL-4. Our data suggest that IL-6 is important as an accessory signal for T cell growth in the CD2 pathway of T cell activation.


This article has been cited by other articles:


Home page
 Biol. Reprod.Home page
G. Soboll, L. Shen, and C. R. Wira
Expression of Toll-Like Receptors (TLR) and Responsiveness to TLR Agonists by Polarized Mouse Uterine Epithelial Cells in Culture
Biol Reprod, July 1, 2006; 75(1): 131 - 139.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
T. M. Schaefer, J. V. Fahey, J. A. Wright, and C. R. Wira
Innate Immunity in the Human Female Reproductive Tract: Antiviral Response of Uterine Epithelial Cells to the TLR3 Agonist Poly(I:C)
J. Immunol., January 15, 2005; 174(2): 992 - 1002.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
A. C. La Flamme, A. S. MacDonald, and E. J. Pearce
Role of IL-6 in Directing the Initial Immune Response to Schistosome Eggs
J. Immunol., March 1, 2000; 164(5): 2419 - 2426.
[Abstract] [Full Text] [PDF]

Home page
 Infect. Immun.Home page
I. S. Leal, B. Smedegard, P. Andersen, and R. Appelberg
Interleukin-6 and Interleukin-12 Participate in Induction of a Type 1 Protective T-Cell Response during Vaccination with a Tuberculosis Subunit Vaccine
Infect. Immun., November 1, 1999; 67(11): 5747 - 5754.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1990 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1990 by The American Association of Immunologists, Inc. All rights reserved.