HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

J. Biol. Chem., Vol. 279, Issue 22, 23394-23404, May 28, 2004

This Article Full Text Full Text (PDF) All Versions of this Article: 279/22/23394    most recent M313096200v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Podojil, J. R. Articles by Sanders, V. M. Search for Related Content PubMed PubMed Citation Articles by Podojil, J. R. Articles by Sanders, V. M. Social Bookmarking                      What's this?

CD86 and ₂-Adrenergic Receptor Signaling Pathways, Respectively, Increase Oct-2 and OCA-B Expression and Binding to the 3'-IgH Enhancer in B Cells^*

Joseph R. Podojil, Nicholas W. Kin, and Virginia M. Sanders¶

From the Department of Molecular Virology, Immunology, and Medical Genetics, The Ohio State University, Columbus, Ohio 43210

Stimulation of CD86 (formerly known as B7-2) and/or the ₂-adrenergic receptor on a CD40 ligand/interleukin-4-activated B cell increased the rate of mature IgG₁ transcription. To identify the mechanism responsible for this effect, we determined whether CD86 and/or ₂-adrenergic receptor stimulation regulated transcription factor expression and binding to the 3'-IgH enhancer in vitro and in vivo. We showed that CD86 stimulation increased the nuclear localization of NF-B1 (p50) and phosphorylated RelA (p65) and increased Oct-2 expression and binding to the 3'-IgH enhancer, in a protein kinase C-dependent manner. These effects were lost when CD86-deficient or NF-B1-deficient B cells were used. CD86 stimulation also increased the level of IB- phosphorylation but in a protein kinase C-independent manner. ₂-Adrenergic receptor stimulation increased CREB phosphorylation, OCA-B expression, and OCA-B binding to the 3'-IgH enhancer in a protein kinase A-dependent manner, an effect lost when ₂-adrenergic receptor-deficient B cells were used. Also, the ₂-adrenergic receptor-induced increase in the level of mature IgG₁ transcript was lost when OCA-B-deficient B cells were used. These data are the first to show that CD86 stimulation up-regulates the expression of the transcription factor Oct-2 in a protein kinase C- and NF-B1-dependent manner, and that ₂-adrenergic receptor stimulation up-regulates the expression of the coactivator OCA-B in a protein kinase A-dependent manner to cooperate with Oct-2 binding to the 3'-IgH enhancer.

Received for publication, December 1, 2003 , and in revised form, February 17, 2004.

^* This work was supported in part by National Institutes of Health Grants AI37326 and AI47420. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Performed this work as part of the dissertation research as predoctoral student in the Department of Cell Biology, Neurobiology, and Anatomy, Loyola University Medical Center, Maywood, IL 60153.

Recipient of National Institutes of Health Training Grant T32 AI55411.

^¶ To whom correspondence should be addressed: Dept. of Molecular Virology, Immunology, and Medical Genetics, The Ohio State University, 2194 Graves Hall, 333 West 10th St., Columbus, OH 43210. Tel.: 614-292-3349; Fax: 614-292-9805; E-mail: Sanders.302{at}osu.edu.

CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

				N. W. Kin and V. M. Sanders CD86 Regulates IgG1 Production via a CD19-Dependent Mechanism J. Immunol., August 1, 2007; 179(3): 1516 - 1523. [Abstract] [Full Text] [PDF]

				G. Pongratz, J. W. McAlees, D. H. Conrad, R. S. Erbe, K. M. Haas, and V. M. Sanders The Level of IgE Produced by a B Cell Is Regulated by Norepinephrine in a p38 MAPK- and CD23-Dependent Manner. J. Immunol., September 1, 2006; 177(5): 2926 - 2938. [Abstract] [Full Text] [PDF]

				J. R. Podojil, A. P. Kohm, and S. D. Miller CD4+ T Cell Expressed CD80 Regulates Central Nervous System Effector Function and Survival during Experimental Autoimmune Encephalomyelitis. J. Immunol., September 1, 2006; 177(5): 2948 - 2958. [Abstract] [Full Text] [PDF]

				N. W. Kin and V. M. Sanders It takes nerve to tell T and B cells what to do J. Leukoc. Biol., June 1, 2006; 79(6): 1093 - 1104. [Abstract] [Full Text] [PDF]

				N. W. Kin and V. M. Sanders CD86 Stimulation on a B Cell Activates the Phosphatidylinositol 3-Kinase/Akt and Phospholipase C{gamma}2/Protein Kinase C{alpha}beta Signaling Pathways. J. Immunol., June 1, 2006; 176(11): 6727 - 6735. [Abstract] [Full Text] [PDF]

				J. Caron, L. Lariviere, M. Nacache, M. Tam, M. M. Stevenson, C. McKerly, P. Gros, and D. Malo Influence of Slc11a1 on the Outcome of Salmonella enterica Serovar Enteritidis Infection in Mice Is Associated with Th Polarization. Infect. Immun., May 1, 2006; 74(5): 2787 - 2802. [Abstract] [Full Text] [PDF]