BOB.1OBF.1 deficiency affects marginal-zone B-cell compartment
Апстракт
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 change...s 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.
Извор:
Molecular and Cellular Biology, 2002, 22, 23, 8320-8331Издавач:
- Amer Soc Microbiology, Washington
DOI: 10.1128/MCB.22.23.8320-8331.2002
ISSN: 0270-7306
PubMed: 12417733
WoS: 000179190600020
Scopus: 2-s2.0-0036889190
Институција/група
rFASPERTY - 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 . .