@article{
author = "Samardžić, T. and Marinković, Dragan and Nielsen, P.J. and Nitschke, L. and Wirth, Thomas",
year = "2002",
abstract = "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 It 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.",
publisher = "Amer Soc Microbiology, Washington",
journal = "Molecular and Cellular Biology",
title = "BOB.1OBF.1 deficiency affects marginal-zone B-cell compartment",
pages = "8331-8320",
number = "23",
volume = "22",
doi = "10.1128/MCB.22.23.8320-8331.2002"
}