The JI PBL Intereron Source
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 Hancock, W. W.
Right arrow Articles by Cotran, R. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hancock, W. W.
Right arrow Articles by Cotran, R. S.
Right arrowPubmed/NCBI databases
*Substance via MeSH
Medline Plus Health Information
*Lung Diseases
*Sarcoidosis

The Journal of Immunology, Vol 138, Issue 1 185-191, Copyright © 1987 by American Association of Immunologists


ARTICLES

Interleukin 2 receptors are expressed by alveolar macrophages during pulmonary sarcoidosis and are inducible by lymphokine treatment of normal human lung macrophages, blood monocytes, and monocyte cell lines

WW Hancock, WA Muller and RS Cotran

Expression of receptors for IL 2 was believed initially to be restricted to T cells after their activation by IL 1 and antigen. However, recently IL 2 receptors (IL 2R) were demonstrated on activated B cells by using an anti-IL 2R monoclonal antibody (anti-Tac). In this study, we examined the capacity of cultured human alveolar macrophages, blood monocytes, and myelomonocytic (HL-60) or monoblast (U937) cell lines to bind three different anti-IL 2R monoclonal antibodies before or after stimulation with the monocyte-activating agents IFN-gamma, LPS, phorbol ester, or lymphokine-containing conditioned medium. For each of the four cell populations examined, resting unstimulated cells bound little or no anti-IL 2R antibody, as shown independently by quantitative cell binding assay and by immunoperoxidase labeling. By contrast, incubation with recombinant IFN-gamma, conditioned medium, or to a lesser extent, native or recombinant IL 2 itself, resulted in a significant enhancement of anti-IL 2 receptor monoclonal antibody binding by all four populations, whereas LPS, PMA, or IL 1 had no effect. In addition, membrane binding of anti-Tac antibody, similar to that seen after stimulation of normal lung macrophages with IFN-gamma, was detected by using macrophages obtained by bronchoalveolar lavage of five patients with active pulmonary sarcoidosis. These findings are consistent with the expression of a functional IL 2R on activated cells of the monocyte lineage, since anti-Tac binding to IFN-gamma-treated HL- 60 cells was inhibited by addition of excess IL-2; specific binding of anti-IL 2 monoclonal antibodies was detected in the presence of exogenous IL 2; and a 50 to 55 kD molecule was immunoprecipitated from both activated lung macrophages and T lymphoblasts by using anti-Tac antibody. We conclude that human mononuclear phagocytes can be induced by lymphokines to express IL 2R, and that such IL 2R+ macrophages can be detected in vivo during inflammation.


This article has been cited by other articles:


Home page
CVIHome page
D. T. Nardelli, T. F. Warner, S. M. Callister, and R. F. Schell
Anti-CD25 Antibody Treatment of Mice Vaccinated and Challenged with Borrelia spp. Does Not Exacerbate Arthritis but Inhibits Borreliacidal Antibody Production.
Clin. Vaccine Immunol., August 1, 2006; 13(8): 884 - 891.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Physiol. Lung Cell. Mol. Physiol.Home page
Y. Katagiri, T. Ito, S. Saino-Saito, Y. Hozumi, A. Suwabe, K. Otake, M. Sata, H. Kondo, F. Sakane, H. Kanoh, et al.
Expression and localization of diacylglycerol kinase isozymes and enzymatic features in rat lung
Am J Physiol Lung Cell Mol Physiol, June 1, 2005; 288(6): L1171 - L1178.
[Abstract] [Full Text] [PDF]


Home page
Circ. Res.Home page
R. Rabinovici, G. Feuerstein, F. Abdullah, M. Whiteford, P. Borboroglu, E. Sheikh, D.-R. Phillip, P. Ovadia, L. Bobroski, O. Bagasra, et al.
Locally Produced Tumor Necrosis Factor-{alpha} Mediates Interleukin-2Induced Lung Injury
Circ. Res., February 1, 1996; 78(2): 329 - 336.
[Abstract] [Full Text]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1987 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1987 by The American Association of Immunologists, Inc. All rights reserved.