Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (52)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Braun, D.
Right arrow Articles by Demengeot, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Braun, D.
Right arrow Articles by Demengeot, J.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

International Immunology, Vol. 14, No. 4, pp. 411-419, April 2002
© 2002 Japanese Society for Immunology

IFN-{alpha}/ß enhances BCR-dependent B cell responses

Déborah Braun1,2, Iris Caramalho1 and Jocelyne Demengeot1

1 Instituto Gulbenkian de Ciência, Rua da Quinta Grande #6, 2781 Oeiras, Portugal 2 Present address: Laboratoire d’Immunorégulation, Centre de Recherche du CHUM, Hôpital Notre-Dame, 1560 Sherbrooke Est., Montréal H2L4M1 Canada

Correspondence to: J. Demengeot; E-mail: jocelyne{at}igc.gulbenkian.pt
Transmitting editor: T. Hünig

Type I interferon (IFN-I) is constitutively produced in the bone marrow (BM), and induced at sites of inflammation and following infection by viruses or microorganisms. We have previously shown that IFN-I regulates the generation and selection of normal B cell populations in the BM. In the present work, we assess the effects of IFN-I on mature B cell function by monitoring the responses of IFN-{alpha}/ß-treated murine splenic B cells to apoptotic, mitogenic and activating stimuli. A similar analysis is performed on BM mature B cells obtained from wild-type or IFN-I receptor-deficient mice. IFN-{alpha}/ß is shown to induce B cells to a state of partial activation characterized by the up-regulation of CD69, CD86 and CD25 molecules in the absence of either proliferation or terminal differentiation. B cells treated with IFN-{alpha}/ß show an increased survival and resistance to Fas-mediated apoptosis. IFN-{alpha}/ß also enhances B cell responses to BCR ligation such as calcium fluxes, IgM internalization, induction of activation markers and proliferation. These results indicate that in addition to its inhibitory effect on viral replication and T cell apoptosis, IFN-{alpha}/ß plays an essential role during an inflammatory response by lowering the threshold for B cell induction, thereby promoting fast and polyclonal antibody responses.

Keywords: B lymphocytes, cellular activation, cytokines, immuno-modulation


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Rheumatology (Oxford)Home page
B. Rhodes and T. J. Vyse
The genetics of SLE: an update in the light of genome-wide association studies
Rheumatology, July 8, 2008; (2008) ken247v1.
[Abstract] [Full Text] [PDF]

Home page
 J. Exp. Med.Home page
T. Saito and M. Gale Jr.
Differential recognition of double-stranded RNA by RIG-I-like receptors in antiviral immunity
J. Exp. Med., July 7, 2008; 205(7): 1523 - 1527.
[Abstract] [Full Text] [PDF]

Home page
 Ann. N. Y. Acad. Sci.Home page
R. LE PANSE, G. CIZERON-CLAIRAC, M. CUVELIER, F. TRUFFAULT, J. BISMUTH, P. NANCY, N. K. DE ROSBO, and S. BERRIH-AKNIN
Regulatory and Pathogenic Mechanisms in Human Autoimmune Myasthenia Gravis
Ann. N.Y. Acad. Sci., June 1, 2008; 1132(1): 135 - 142.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
S. L. Day, I. A. Ramshaw, A. J. Ramsay, and C. Ranasinghe
Differential Effects of the Type I Interferons {alpha}4, {beta}, and {epsilon} on Antiviral Activity and Vaccine Efficacy
J. Immunol., June 1, 2008; 180(11): 7158 - 7166.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
S. Kunz, K. Oberle, A. Sander, C. Bogdan, and U. Schleicher
Lymphadenopathy in a Novel Mouse Model of Bartonella-Induced Cat Scratch Disease Results from Lymphocyte Immigration and Proliferation and Is Regulated by Interferon-{alpha}/{beta}
Am. J. Pathol., April 1, 2008; 172(4): 1005 - 1018.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
N.-H. Chang, T. McKenzie, G. Bonventi, C. Landolt-Marticorena, P. R. Fortin, D. Gladman, M. Urowitz, and J. E. Wither
Expanded Population of Activated Antigen-Engaged Cells within the Naive B Cell Compartment of Patients with Systemic Lupus Erythematosus
J. Immunol., January 15, 2008; 180(2): 1276 - 1284.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
J. E. Butler, C. D. Lemke, P. Weber, M. Sinkora, and K. M. Lager
Antibody Repertoire Development in Fetal and Neonatal Piglets: XIX. Undiversified B Cells with Hydrophobic HCDR3s Preferentially Proliferate in the Porcine Reproductive and Respiratory Syndrome
J. Immunol., May 15, 2007; 178(10): 6320 - 6331.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
P. Bach, E. Kamphuis, B. Odermatt, G. Sutter, C. J. Buchholz, and U. Kalinke
Vesicular Stomatitis Virus Glycoprotein Displaying Retrovirus-Like Particles Induce a Type I IFN Receptor-Dependent Switch to Neutralizing IgG Antibodies
J. Immunol., May 1, 2007; 178(9): 5839 - 5847.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
W. L. W. Chang, E. S. Coro, F. C. Rau, Y. Xiao, D. J. Erle, and N. Baumgarth
Influenza Virus Infection Causes Global Respiratory Tract B Cell Response Modulation via Innate Immune Signals
J. Immunol., February 1, 2007; 178(3): 1457 - 1467.
[Abstract] [Full Text] [PDF]

Home page
 Infect. Immun.Home page
T. Mahieu and C. Libert
Should We Inhibit Type I Interferons in Sepsis?
Infect. Immun., January 1, 2007; 75(1): 22 - 29.
[Full Text] [PDF]

Home page
 BloodHome page
E. Kamphuis, T. Junt, Z. Waibler, R. Forster, and U. Kalinke
Type I interferons directly regulate lymphocyte recirculation and cause transient blood lymphopenia
Blood, November 15, 2006; 108(10): 3253 - 3261.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
M. Alsharifi, M. Regner, R. Blanden, M. Lobigs, E. Lee, A. Koskinen, and A. Mullbacher
Exhaustion of Type I Interferon Response following an Acute Viral Infection.
J. Immunol., September 1, 2006; 177(5): 3235 - 3241.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
R. Asokan, J. Hua, K. A. Young, H. J. Gould, J. P. Hannan, D. M. Kraus, G. Szakonyi, G. J. Grundy, X. S. Chen, M. K. Crow, et al.
Characterization of Human Complement Receptor Type 2 (CR2/CD21) as a Receptor for IFN-{alpha}: A Potential Role in Systemic Lupus Erythematosus
J. Immunol., July 1, 2006; 177(1): 383 - 394.
[Abstract] [Full Text] [PDF]

Home page
 J. Virol.Home page
C. B. Lopez, J. S. Yount, T. Hermesh, and T. M. Moran
Sendai Virus Infection Induces Efficient Adaptive Immunity Independently of Type I Interferons
J. Virol., May 1, 2006; 80(9): 4538 - 4545.
[Abstract] [Full Text] [PDF]

Home page
 J. Virol.Home page
C. B. Lopez, J. S. Yount, and T. M. Moran
Toll-like receptor-independent triggering of dendritic cell maturation by viruses.
J. Virol., April 1, 2006; 80(7): 3128 - 3134.
[Full Text] [PDF]

Home page
 J. Immunol.Home page
E. S. Coro, W. L. W. Chang, and N. Baumgarth
Type I IFN Receptor Signals Directly Stimulate Local B Cells Early following Influenza Virus Infection
J. Immunol., April 1, 2006; 176(7): 4343 - 4351.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
A. Le Bon, C. Thompson, E. Kamphuis, V. Durand, C. Rossmann, U. Kalinke, and D. F. Tough
Cutting Edge: Enhancement of Antibody Responses Through Direct Stimulation of B and T Cells by Type I IFN
J. Immunol., February 15, 2006; 176(4): 2074 - 2078.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
M. Alsharifi, M. Lobigs, M. Regner, E. Lee, A. Koskinen, and A. Mullbacher
Type I Interferons Trigger Systemic, Partial Lymphocyte Activation in Response to Viral Infection
J. Immunol., October 1, 2005; 175(7): 4635 - 4640.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
C. M. Grimaldi, R. Hicks, and B. Diamond
B Cell Selection and Susceptibility to Autoimmunity
J. Immunol., February 15, 2005; 174(4): 1775 - 1781.
[Abstract] [Full Text] [PDF]

Home page
 Innate ImmunityHome page
J. Vollmer, M. Jurk, U. Samulowitz, G. Lipford, A. Forsbach, M. Wullner, S. Tluk, H. Hartmann, A. Kritzler, C. Muller, et al.
CpG oligodeoxynucleotides stimulate IFN-{gamma}-inducible protein-10 production in human B cells
Innate Immunity, December 1, 2004; 10(6): 431 - 438.
[Abstract] [PDF]

Home page
 J. Immunol.Home page
Z.-X. Lian, K. Kikuchi, G.-X. Yang, A. A. Ansari, S. Ikehara, and M. E. Gershwin
Expansion of Bone Marrow IFN-{alpha}-Producing Dendritic Cells in New Zealand Black (NZB) Mice: High Level Expression of TLR9 and Secretion of IFN-{alpha} in NZB Bone Marrow
J. Immunol., October 15, 2004; 173(8): 5283 - 5289.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
J. D. Hron and S. L. Peng
Type I IFN Protects Against Murine Lupus
J. Immunol., August 1, 2004; 173(3): 2134 - 2142.
[Abstract] [Full Text] [PDF]

Home page
 Int ImmunolHome page
D. Yuan, R. Bibi, and T. Dang
The role of adjuvant on the regulatory effects of NK cells on B cell responses as revealed by a new model of NK cell deficiency
Int. Immunol., May 1, 2004; 16(5): 707 - 716.
[Abstract] [Full Text] [PDF]

Home page
 J. Exp. Med.Home page
M.-L. Santiago-Raber, R. Baccala, K. M. Haraldsson, D. Choubey, T. A. Stewart, D. H. Kono, and A. N. Theofilopoulos
Type-I Interferon Receptor Deficiency Reduces Lupus-like Disease in NZB Mice
J. Exp. Med., March 17, 2003; 197(6): 777 - 788.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.