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 Tanaka, T.
Right arrow Articles by Paul, W. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tanaka, T.
Right arrow Articles by Paul, W. E.

The Journal of Immunology, Vol 146, Issue 11 3831-3839, Copyright © 1991 by American Association of Immunologists


ARTICLES

IL-4 increases IL-2 production by T cells in response to accessory cell- independent stimuli

T Tanaka, SZ Ben-Sasson and WE Paul
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892.

Freshly prepared, highly purified T cells from naive mice failed to produce IL-2 in response to soluble anti-CD3 antibody or to Con A and produced only small amounts of IL-2 in response to anti-CD3 coated on the surface of microwells. IL-2 production in response to soluble anti- CD3 or to Con A required the addition of accessory cells. By contrast, the addition of IL-4 strikingly enhanced the production of IL-2 by plate-bound anti-CD3-stimulated T cells in the absence or the presence of added accessory cells. Furthermore, anti-IL-4 mAb inhibited IL-2 production by anti-CD3-stimulated T cells, which indicates that endogenously produced IL-4 was important in IL-2 production by T cells to plate-bound anti-CD3. The capacity of IL-4 to enhance and of anti-IL- 4 to inhibit IL-2 production in response to plate-bound anti-CD3 was also observed with both unstimulated T cells and with T cells that had been previously stimulated with anti-CD3 antibody. When activated T cells were restimulated with anti-CD3, the effect of IL-4 in enhancing IL-2 production was detectable within 6 to 8 h after restimulation. The effect of IL-4 on IL-2 production was not due to prolongation of survival or to enhanced proliferation of T cells. Northern blot analysis showed that T cells treated with anti-CD3 plus IL-4 had more than 10-fold more IL-2 mRNA than did T cells treated with anti-CD3 plus anti-IL-4; this was observed within 6 h of stimulation under certain circumstances. The increased level of IL-2 mRNA by IL-4 was achieved without any change in message half-life, suggesting that IL-4 enhances transcriptional activation of the IL-2 gene in such cells. These results lead to the conclusion that IL-4 has a critical role in IL-2 production in response to accessory cell-independent stimuli (plate- bound anti-CD3 antibody), although it is not essential to IL-2 production in response to accessory cell-dependent stimuli (soluble anti-CD3 and Con A).


This article has been cited by other articles:


Home page
J. Immunol.Home page
K. Lingnau, P. Hoehn, S. Kerdine, S. Koelsch, C. Neudoerfl, N. Palm, E. Ruede, and E. Schmitt
IL-4 in Combination with TGF-{beta} Favors an Alternative Pathway of Th1 Development Independent of IL-12
J. Immunol., November 1, 1998; 161(9): 4709 - 4718.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1991 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1991 by The American Association of Immunologists, Inc. All rights reserved.