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 Francis, M. L.
Right arrow Articles by Meltzer, M. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Francis, M. L.
Right arrow Articles by Meltzer, M. S.

The Journal of Immunology, Vol 156, Issue 7 2481-2487, Copyright © 1996 by American Association of Immunologists

ARTICLES

Loss ability to produce IFN-alpha in response to HIV-1 as monocytes differentiate into macrophages. Induction through a mechanism independent of double-stranded RNA

ML Francis, XS Fan and MS Meltzer
Section on Rheumatology, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC 27157, USA.

IFN-alpha is an antiviral cytokine detected in plasma of HIV-1-infected patients during acute viremia and during late-stage disease. Monocytes produced IFN-alpha in response to HIV-1:1) IFN-alpha was produced predominantly by adherent cells; 2) depleting CD14+ cells nearly abolished HIV-1-induced IFN-alpha production; and 3) intracytoplasmic IFN-alpha was detected in CD14+ cells. During cell culture, monocytes differentiated into macrophages and lost their ability to produce IFN- alpha when challenged with HIV-1. These cells remained capable of producing IFN-alpha in response to other stimuli such as poly(I:C), a synthetic dsRNA. Thus, we examined two negative-stranded RNA viruses that have dsRNA intermediates, Newcastle disease virus and Sendai virus, and a DNA virus, herpes simplex virus type I (HSV-1). Macrophages lost their ability to produce IFN-alpha in response to HSV- 1, but not to Sendai virus or to Newcastle disease virus. Thus, HIV-1 and other viruses were capable of inducing IFN-alpha through a mechanism that was independent of dsRNA. In conclusion, these data suggest that there are dsRNA-dependent and -independent mechanisms for the induction of IFN-alpha production, and that as monocytes differentiate into macrophages, they selectively lose their ability to produce IFN-alpha through the dsRNA-independent mechanism.


This article has been cited by other articles:


Home page
 J. Leukoc. Biol.Home page
D. L. Brassard, M. J. Grace, and R. W. Bordens
Interferon-{alpha} as an immunotherapeutic protein
J. Leukoc. Biol., April 1, 2002; 71(4): 565 - 581.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
P. Hermann, M. Rubio, T. Nakajima, G. Delespesse, and M. Sarfati
IFN-{alpha} Priming of Human Monocytes Differentially Regulates Gram-Positive and Gram-Negative Bacteria-Induced IL-10 Release and Selectively Enhances IL-12p70, CD80, and MHC Class I Expression
J. Immunol., August 15, 1998; 161(4): 2011 - 2018.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1996 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1996 by The American Association of Immunologists, Inc. All rights reserved.