The Journal of Experimental Medicine
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Published 15 August 2005. doi:10.1084/jem.20050575
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 202, Number 4, 505-516
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ARTICLE

 XBP-1 specifically promotes IgM synthesis and secretion, but is dispensable for degradation of glycoproteins in primary B cells

Boaz Tirosh1, Neal N. Iwakoshi2, Laurie H. Glimcher2, and Hidde L. Ploegh1

1 Department of Pathology, Harvard Medical School
2 Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, MA 02115

CORRESPONDENCE Hidde L. Ploegh: hidde_ploegh{at}hms.harvard.edu

Differentiation of B cells into plasma cells requires X-box binding protein–1 (XBP-1). In the absence of XBP-1, B cells develop normally, but very little immunoglobulin is secreted. XBP-1 controls the expression of a large set of genes whose products participate in expansion of the endoplasmic reticulum (ER) and in protein trafficking. We define a new role for XBP-1 in exerting selective translational control over high and sustained levels of immunoglobulin M (IgM) synthesis. XBP-1–/– and XBP-1+/+ primary B cells synthesize IgM at comparable levels at the onset of stimulation with lipopolysaccharide or CpG. However, later there is a profound depression in synthesis of IgM in XBP-1–/– B cells, notwithstanding similar levels of µmRNA. In marked contrast, lack of XBP-1 does not affect synthesis and trafficking of other glycoproteins, or of immunoglobulin light chains. Contrary to expectation, degradation of proteins from the ER, using TCR{alpha} or US11-mediated degradation of class I major histocompatibility complex molecules as substrates, is normal in XBP-1–/– B cells. Furthermore, degradation of membrane µ was unaffected by enforced expression of XBP-1. We conclude that in primary B cells, the XBP-1 pathway promotes synthesis and secretion of IgM, but does not seem to be involved in the degradation of ER proteins, including that of µ chains themselves.

Abbreviations used: µm, membrane µ; µs, secretory µ; ATF, activating transcription factor; EDEM, ER degradation enhancing {alpha}-mannosidase-like protein; HC, class I MHC heavy chain; IRES, internal ribosome entry site; PERK, PKR-like endoplasmic reticulum eIF2{alpha} kinase; SRP, signal recognition particle; UPR, unfolded protein response; XBP-1, X-box binding protein 1; XBP-1s, spliced XBP-1.


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