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 Freedman, A. S.
Right arrow Articles by Nadler, L. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Freedman, A. S.
Right arrow Articles by Nadler, L. M.

The Journal of Immunology, Vol 141, Issue 10 3398-3404, Copyright © 1988 by American Association of Immunologists


ARTICLES

Pre-exposure of human B cells to recombinant IL-1 enhances subsequent proliferation

AS Freedman, G Freeman, J Whitman, J Segil, J Daley and LM Nadler
Division of Tumor Immunology, Dana-Farber Cancer Institute, Boston, MA 02115.

The reported effects of the monocyte-derived cytokine IL-1 on human B lymphocytes are both varied and controversial. IL-1 has been reported to augment both proliferation and Ig secretion of previously activated human B cells. In the present study highly purified splenic B cells were cultured with rIL-1 before, simultaneously with, and after the addition of the polyclonal B cell mitogen, anti-Ig. rIL-1 had no significant effect on B cell proliferation when added simultaneously with or after B cell activation with anti-Ig. However, incubation of splenic B cells with rIL-1 for 24 h before stimulation with anti-Ig appeared to enhance mitogenesis. With the observation that rIL-1 exerted effects on resting B cells, the effect of rIL-1 on several events which accompany B cell activation was examined. rIL-1 failed to stimulate RNA synthesis, effect increases in cell size or intracellular Ca2+ levels, or lead to the hyperexpression of MHC class II or B cell activation Ag. These studies suggest that rIL-1 does not activate B cells but primes them to respond to subsequent activation.


This article has been cited by other articles:


Home page
Int ImmunolHome page
A. Nambu, S. Nakae, and Y. Iwakura
IL-1{beta}, but not IL-1{alpha}, is required for antigen-specific T cell activation and the induction of local inflammation in the delayed-type hypersensitivity responses
Int. Immunol., May 1, 2006; 18(5): 701 - 712.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
S. Itoh, T. Hattori, H. Hayashi, Y. Mizutani, M. Todo, T. Takii, D. Yang, J. C. Lee, S. Matsufuji, Y. Murakami, et al.
Antiproliferative Effect of IL-1 Is Mediated by p38 Mitogen-Activated Protein Kinase in Human Melanoma Cell A375
J. Immunol., June 15, 1999; 162(12): 7434 - 7440.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
R. L. Chelvarajan, N. L. Gilbert, and S. Bondada
Neonatal Murine B Lymphocytes Respond to Polysaccharide Antigens in the Presence of IL-1 and IL-6
J. Immunol., October 1, 1998; 161(7): 3315 - 3324.
[Abstract] [Full Text] [PDF]


Home page
fake Crit Rev Oral Biol MedHome page
E. Gemmell and G. J. Seymour
Cytokines and T Cell Switching
Critical Reviews in Oral Biology & Medicine, January 1, 1994; 5(3): 249 - 279.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1988 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1988 by The American Association of Immunologists, Inc. All rights reserved.