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Molecular and Cellular Biology, December 2002, p. 8320-8331, Vol. 22, No. 23
0270-7306/02/$04.00+0     DOI: 10.1128/MCB.22.23.8320-8331.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

BOB.1/OBF.1 Deficiency Affects Marginal-Zone B-Cell Compartment

Tatjana Samardzic,1 Dragan Marinkovic,1 Peter J. Nielsen,2* Lars Nitschke,3 and Thomas Wirth1

Department of Physiological Chemistry, Ulm University, 89081 Ulm,1 Max Planck Institute for Immunobiology, D-79108 Freiburg,2 Institute for Virology and Immunobiology, Wuerzburg University, 97078 Wuerzburg, Germany3

Received 15 May 2002/ Returned for modification 10 July 2002/ Accepted 4 September 2002

Marginal-zone (MZ) B cells represent a first line of defense against particulate blood-borne antigens. Together with the B1 cells, they are responsible for the early response against type II T-independent antigens. The molecular pathways controlling the development of MZ B cells are only poorly understood. We found that these cells are virtually absent in mice deficient in the BOB.1/OBF.1 coactivator. Loss of these B cells was demonstrated by the lack of cells showing the appropriate cell surface phenotype but also by histological analyses and tri-nitro-phenol-Ficoll capturing. The lack of these cells is a B-cell-intrinsic defect, as shown by bone marrow complementation experiments. We also show that the expression of BOB.1/OBF.1 in peripheral B cells is required for the development of MZ B lymphocytes. Our analysis of BOB.1/OBF.1-deficient splenic B cells reveals alterations in cell motility, tumor necrosis factor receptor expression, and B-cell receptor (BCR) signaling. These changes could contribute to the loss of MZ B lymphocytes by altering the maturation of the cells. Interestingly, development of and BCR signaling in B1 B cells are completely normal in BOB.1/OBF.1 mutant mice.

* Corresponding author. Mailing address for Thomas Wirth: Department of Physiological Chemistry, Ulm University, Albert-Einstein-Allee 11, 89081 Ulm, Germany. Phone: 49 731 502 3270. Fax: 49 761 5108221. E-mail: thomas.wirth{at}medizin.uni-ulm.de. Mailing address for Peter J. Nielsen: Max Planck Institute for Immunobiology, Stubeweg 51, D-79108 Freiburg, Germany. Phone: 49 761 5108319. Fax: 49 731 502 2892. E-mail: nielsen{at}immunbio.mpg.de.

Molecular and Cellular Biology, December 2002, p. 8320-8331, Vol. 22, No. 23
0022-538X/02/$04.00+0     DOI: 10.1128/MCB.22.23.8320-8331.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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