| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
(2b) Increases the Expression of Apoptosis Receptor CD95 and Chemokine Receptors CCR1 and CCR3 in Monocytoid Cells1
*
Institute of Human Virology, University of Maryland, Baltimore MD 21201;
Laboratory of Basic Science, National Cancer Institute, National Institutes of Health, Bethesda MD 20814; and
Department of Morphology and Embriology, Human Anatomy Section, Ferrara, Italy
IFN-
-2b, known as potent immune modulator, can either inhibit or
enhance immune cell activity within the tightly regulated
microenvironment of inflammation, depending upon the concentration of
the cytokine and the activation stage of the cell. Chemokine receptors,
which not only mediate chemotaxis of immune cells to the site of
inflammation but also affect cellular activation by transferring
corresponding signals, represent yet another level of immune
regulation. Here we demonstrate that IFN- increases the expression
of CCR1 and CCR3 in primary mononuclear phagocytes, as well as in the
monocytoid cell line U937. Enhanced receptor mRNA expression correlated
with functional readouts such as increased intracellular calcium
mobilization and cell migration in response to ligands. Expression of
CCR2b, CCR4, CCR5, and CXCR4 was unchanged or decreased after IFN-
treatment. These observations indicate a differentially regulated
cellular signaling relationship of IFN- pathways and chemokine
receptor expression. We also provide evidence that, under these
conditions, IFN- treatment increased the expression of CD95 (Fas,
Apo1), resulting in enhanced susceptibility to apoptosis. Taken
together, these data add important information for the rational
application of IFN- (2b) in immune and cancer
therapies.
This article has been cited by other articles:
|
|
 |
|
  P. Joubert, S. Lajoie-Kadoch, M. Welman, S. Dragon, S. Letuvee, B. Tolloczko, A. J. Halayko, A. S. Gounni, K. Maghni, and Q. Hamid Expression and Regulation of CCR1 by Airway Smooth Muscle Cells in Asthma J. Immunol., January 15, 2008; 180(2): 1268 - 1275. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. F. Denny, S. Thacker, H. Mehta, E. C. Somers, T. Dodick, F. J. Barrat, W. J. McCune, and M. J. Kaplan Interferon-{alpha} promotes abnormal vasculogenesis in lupus: a potential pathway for premature atherosclerosis Blood, October 15, 2007; 110(8): 2907 - 2915. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. L Nagpal, Y. Chen, and T. Lin Effects of overexpression of CXCL10 (cytokine-responsive gene-2) on MA-10 mouse Leydig tumor cell steroidogenesis and proliferation J. Endocrinol., December 1, 2004; 183(3): 585 - 594. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. K. Baker, A. R. Pettitt, J. R. Slupsky, H. J. Chen, M. A. Glenn, M. Zuzel, and J. C. Cawley Response of hairy cells to IFN-alpha involves induction of apoptosis through autocrine TNF-alpha and protection by adhesion Blood, June 28, 2002; 100(2): 647 - 653. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Bouchonnet, N. Boechat, M. Bonay, and A. J. Hance Alpha/Beta Interferon Impairs the Ability of Human Macrophages To Control Growth of Mycobacterium bovis BCG Infect. Immun., June 1, 2002; 70(6): 3020 - 3025. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Chawla-Sarkar, D. W. Leaman, and E. C. Borden Preferential Induction of Apoptosis by Interferon (IFN)-{beta} Compared with IFN-{{alpha}}2: Correlation with TRAIL/Apo2L Induction in Melanoma Cell Lines Clin. Cancer Res., June 1, 2001; 7(6): 1821 - 1831. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Zimmermann, B. L. Daugherty, J. L. Kavanaugh, F. Y. El-Awar, E. A. Moulton, and M. E. Rothenberg Analysis of the CC chemokine receptor 3 gene reveals a complex 5' exon organization, a functional role for untranslated exon 1, and a broadly active promoter with eosinophil-selective elements Blood, October 1, 2000; 96(7): 2346 - 2354. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
