Nielsen, P.J.

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  • Nielsen, P.J. (1)
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BOB.1OBF.1 deficiency affects marginal-zone B-cell compartment

Samardžić, T.; Marinković, Dragan; Nielsen, P.J.; Nitschke, L.; Wirth, Thomas

(Amer Soc Microbiology, Washington, 2002)

TY  - JOUR
AU  - Samardžić, T.
AU  - Marinković, Dragan
AU  - Nielsen, P.J.
AU  - Nitschke, L.
AU  - Wirth, Thomas
PY  - 2002
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/28
AB  - 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.
PB  - Amer Soc Microbiology, Washington
T2  - Molecular and Cellular Biology
T1  - BOB.1OBF.1 deficiency affects marginal-zone B-cell compartment
EP  - 8331
IS  - 23
SP  - 8320
VL  - 22
DO  - 10.1128/MCB.22.23.8320-8331.2002
ER  - 
@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"
}
Samardžić, T., Marinković, D., Nielsen, P.J., Nitschke, L.,& Wirth, T.. (2002). BOB.1OBF.1 deficiency affects marginal-zone B-cell compartment. in Molecular and Cellular Biology
Amer Soc Microbiology, Washington., 22(23), 8320-8331.
https://doi.org/10.1128/MCB.22.23.8320-8331.2002
Samardžić T, Marinković D, Nielsen P, Nitschke L, Wirth T. BOB.1OBF.1 deficiency affects marginal-zone B-cell compartment. in Molecular and Cellular Biology. 2002;22(23):8320-8331.
doi:10.1128/MCB.22.23.8320-8331.2002 .
Samardžić, T., Marinković, Dragan, Nielsen, P.J., Nitschke, L., Wirth, Thomas, "BOB.1OBF.1 deficiency affects marginal-zone B-cell compartment" in Molecular and Cellular Biology, 22, no. 23 (2002):8320-8331,
https://doi.org/10.1128/MCB.22.23.8320-8331.2002 . .
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