TY  - JOUR
AU  - Samanta, DN
AU  - Palmetshofer, A
AU  - Marinković, Dragan
AU  - Wirth, Thomas
AU  - Serfling, E
AU  - Nitschke, L.
PY  - 2005
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/37
AB  - Marginal zone (MZ) B cells and peritoneal B-I cells provide a first defense system of thymus-independent Ab responses against foreign pathogens and therefore share a number of functional properties. Recently, development of B-1a cells was shown to be controlled by the transcription factor NFATc1. We show here that mice deficient for NFATc2 and c3 display a distinct lower representation of MZ B cells, which is correlated with a reduced capturing of trinitrophenyl-Ficoll. In contrast, mature follicular B cells from NFATc2/c3(-/-) mice are strongly increased in number. NFATc2/c3-/- B cells exhibit a marked increase in BCR-induced intracellular Ca(2+) mobilization and proliferation. However, trinitrophenyl-Ficoll-specific IgM and IgG3 responses of NFATc2/c3-deficient mice are intact, and chimeric mice reconstituted with NFATc2/3-deficient B cells show a normal number of MZ B cells and normal BCR responses. These observations suggest that the strongly elevated Th2 cytokine milieu in NFATc2/c3-deficient mice leads to a hyperactivation of mature, follicular B cells, whereas MZ B cells are less responsive to these signals.
PB  - Amer Assoc Immunologists, Bethesda
T2  - Journal of Immunology
T1  - B cell hyperresponsiveness and expansion of mature follicular B cells but not of marginal zone B cells in NFATc2/c3 double-deficient mice
EP  - 4802
IS  - 8
SP  - 4797
VL  - 174
DO  - 10.4049/jimmunol.174.8.4797
ER  - 

@article{
author = "Samanta, DN and Palmetshofer, A and Marinković, Dragan and Wirth, Thomas and Serfling, E and Nitschke, L.",
year = "2005",
abstract = "Marginal zone (MZ) B cells and peritoneal B-I cells provide a first defense system of thymus-independent Ab responses against foreign pathogens and therefore share a number of functional properties. Recently, development of B-1a cells was shown to be controlled by the transcription factor NFATc1. We show here that mice deficient for NFATc2 and c3 display a distinct lower representation of MZ B cells, which is correlated with a reduced capturing of trinitrophenyl-Ficoll. In contrast, mature follicular B cells from NFATc2/c3(-/-) mice are strongly increased in number. NFATc2/c3-/- B cells exhibit a marked increase in BCR-induced intracellular Ca(2+) mobilization and proliferation. However, trinitrophenyl-Ficoll-specific IgM and IgG3 responses of NFATc2/c3-deficient mice are intact, and chimeric mice reconstituted with NFATc2/3-deficient B cells show a normal number of MZ B cells and normal BCR responses. These observations suggest that the strongly elevated Th2 cytokine milieu in NFATc2/c3-deficient mice leads to a hyperactivation of mature, follicular B cells, whereas MZ B cells are less responsive to these signals.",
publisher = "Amer Assoc Immunologists, Bethesda",
journal = "Journal of Immunology",
title = "B cell hyperresponsiveness and expansion of mature follicular B cells but not of marginal zone B cells in NFATc2/c3 double-deficient mice",
pages = "4802-4797",
number = "8",
volume = "174",
doi = "10.4049/jimmunol.174.8.4797"
}

Samanta, D., Palmetshofer, A., Marinković, D., Wirth, T., Serfling, E.,& Nitschke, L.. (2005). B cell hyperresponsiveness and expansion of mature follicular B cells but not of marginal zone B cells in NFATc2/c3 double-deficient mice. in Journal of Immunology
Amer Assoc Immunologists, Bethesda., 174(8), 4797-4802.
https://doi.org/10.4049/jimmunol.174.8.4797

Samanta D, Palmetshofer A, Marinković D, Wirth T, Serfling E, Nitschke L. B cell hyperresponsiveness and expansion of mature follicular B cells but not of marginal zone B cells in NFATc2/c3 double-deficient mice. in Journal of Immunology. 2005;174(8):4797-4802.
doi:10.4049/jimmunol.174.8.4797 .

Samanta, DN, Palmetshofer, A, Marinković, Dragan, Wirth, Thomas, Serfling, E, Nitschke, L., "B cell hyperresponsiveness and expansion of mature follicular B cells but not of marginal zone B cells in NFATc2/c3 double-deficient mice" in Journal of Immunology, 174, no. 8 (2005):4797-4802,
https://doi.org/10.4049/jimmunol.174.8.4797 . .

TY  - JOUR
AU  - Amano, H.
AU  - Amano, E.
AU  - Moll, T.
AU  - Marinković, Dragan
AU  - Ibnou-Zekri, N
AU  - Martinez-Soria, E.
AU  - Semac, I
AU  - Wirth, Thomas
AU  - Nitschke, L.
AU  - Izui, S
PY  - 2003
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/32
AB  - The accelerated development of systemic lupus erythematosus (SLE) in BXSB male mice is associated with the presence of an as yet unidentified mutant gene, Yaa (Y-linked autoimmune acceleration). In view of a possible role of marginal zone (MZ) B cells in murine SLE, we have explored whether the expression of the Yaa mutation affects the differentiation of MZ and follicular B cells, thereby implicating the acceleration of the disease. In this study, we show that both BXSB and C57BL/6 Yaa mice, including two different substrains of BXSB Yaa males that are protected from SLE, displayed an impaired development of MZ B cells early in life. Studies in bone marrow chimeras revealed that the loss of MZ B cells resulted from a defect intrinsic to B cells expressing the Yaa mutation. The lack of selective expansion of MZ B cells in diseased BXSB Yaa males strongly argues against a major role of MZ B cells in the generation of pathogenic autoantibodies in the BXSB model of SLE. Furthermore, a comparative analysis with mice deficient in CD22 or expressing an IgM anti-trinitrophenyl/DNA transgene suggests that the hyperreactive phenotype of Yaa B cells, as judged by a markedly increased spontaneous IgM secretion, is likely to contribute to the enhanced maturation toward follicular B cells and the block in the MZ B cell generation.
PB  - Amer Assoc Immunologists, Bethesda
T2  - Journal of Immunology
T1  - The Yaa mutation promoting murine lupus causes defective development of marginal zone B cells
EP  - 2301
IS  - 5
SP  - 2293
VL  - 170
DO  - 10.4049/jimmunol.170.5.2293
ER  - 

@article{
author = "Amano, H. and Amano, E. and Moll, T. and Marinković, Dragan and Ibnou-Zekri, N and Martinez-Soria, E. and Semac, I and Wirth, Thomas and Nitschke, L. and Izui, S",
year = "2003",
abstract = "The accelerated development of systemic lupus erythematosus (SLE) in BXSB male mice is associated with the presence of an as yet unidentified mutant gene, Yaa (Y-linked autoimmune acceleration). In view of a possible role of marginal zone (MZ) B cells in murine SLE, we have explored whether the expression of the Yaa mutation affects the differentiation of MZ and follicular B cells, thereby implicating the acceleration of the disease. In this study, we show that both BXSB and C57BL/6 Yaa mice, including two different substrains of BXSB Yaa males that are protected from SLE, displayed an impaired development of MZ B cells early in life. Studies in bone marrow chimeras revealed that the loss of MZ B cells resulted from a defect intrinsic to B cells expressing the Yaa mutation. The lack of selective expansion of MZ B cells in diseased BXSB Yaa males strongly argues against a major role of MZ B cells in the generation of pathogenic autoantibodies in the BXSB model of SLE. Furthermore, a comparative analysis with mice deficient in CD22 or expressing an IgM anti-trinitrophenyl/DNA transgene suggests that the hyperreactive phenotype of Yaa B cells, as judged by a markedly increased spontaneous IgM secretion, is likely to contribute to the enhanced maturation toward follicular B cells and the block in the MZ B cell generation.",
publisher = "Amer Assoc Immunologists, Bethesda",
journal = "Journal of Immunology",
title = "The Yaa mutation promoting murine lupus causes defective development of marginal zone B cells",
pages = "2301-2293",
number = "5",
volume = "170",
doi = "10.4049/jimmunol.170.5.2293"
}

Amano, H., Amano, E., Moll, T., Marinković, D., Ibnou-Zekri, N., Martinez-Soria, E., Semac, I., Wirth, T., Nitschke, L.,& Izui, S.. (2003). The Yaa mutation promoting murine lupus causes defective development of marginal zone B cells. in Journal of Immunology
Amer Assoc Immunologists, Bethesda., 170(5), 2293-2301.
https://doi.org/10.4049/jimmunol.170.5.2293

Amano H, Amano E, Moll T, Marinković D, Ibnou-Zekri N, Martinez-Soria E, Semac I, Wirth T, Nitschke L, Izui S. The Yaa mutation promoting murine lupus causes defective development of marginal zone B cells. in Journal of Immunology. 2003;170(5):2293-2301.
doi:10.4049/jimmunol.170.5.2293 .

Amano, H., Amano, E., Moll, T., Marinković, Dragan, Ibnou-Zekri, N, Martinez-Soria, E., Semac, I, Wirth, Thomas, Nitschke, L., Izui, S, "The Yaa mutation promoting murine lupus causes defective development of marginal zone B cells" in Journal of Immunology, 170, no. 5 (2003):2293-2301,
https://doi.org/10.4049/jimmunol.170.5.2293 . .

TY  - JOUR
AU  - Brunner, C
AU  - Marinković, Dragan
AU  - Klein, J
AU  - Samardžić, T.
AU  - Nitschke, L.
AU  - Wirth, Thomas
PY  - 2003
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/31
AB  - Mice deficient for the transcriptional coactivator BOB.1/OBF.1 show several defects in B cell differentiation. Numbers of immature transitional B cells in the bone marrow are reduced and fewer B cells reach the periphery. Furthermore, germinal center B cells are absent and marginal zone (MZ) B lymphocytes are markedly reduced. Increased levels of B cell apoptosis in these mice prompted us to analyze expression and function of antiapoptotic proteins. Bcl2 expression is strongly reduced in BOB.1/OBF.1-deficient pre-B cells. When BOB.1/OBF.1-deficient mice were crossed with Bcl2-transgenic mice, B cell development in the bone marrow and numbers of B cells in peripheral lymphoid organs were normalized. However, neither germinal center B cells nor MZ B cells were rescued. Additionally, Bcl2 did not rescue the defects in signaling and affinity maturation found in BOB.1/OBF.1-deficient mice. Interestingly, Bcl2-transgenic mice by themselves show an MZ B cell defect. Virtually no functional MZ B cells were detected in these mice. In contrast, mice deficient for Bcl2 show a relative increase in MZ B cell numbers, indicating a previously undetected function of Bcl2 for this B cell compartment.
PB  - Rockefeller Univ Press, New York
T2  - Journal of Experimental Medicine
T1  - B cell-specific transgenic expression of Bcl2 rescues early B lymphopoiesis but not B cell responses in BOB.1/OBF.1-deficient mice
EP  - 1211
IS  - 9
SP  - 1205
VL  - 197
DO  - 10.1084/jem.20022014
ER  - 

@article{
author = "Brunner, C and Marinković, Dragan and Klein, J and Samardžić, T. and Nitschke, L. and Wirth, Thomas",
year = "2003",
abstract = "Mice deficient for the transcriptional coactivator BOB.1/OBF.1 show several defects in B cell differentiation. Numbers of immature transitional B cells in the bone marrow are reduced and fewer B cells reach the periphery. Furthermore, germinal center B cells are absent and marginal zone (MZ) B lymphocytes are markedly reduced. Increased levels of B cell apoptosis in these mice prompted us to analyze expression and function of antiapoptotic proteins. Bcl2 expression is strongly reduced in BOB.1/OBF.1-deficient pre-B cells. When BOB.1/OBF.1-deficient mice were crossed with Bcl2-transgenic mice, B cell development in the bone marrow and numbers of B cells in peripheral lymphoid organs were normalized. However, neither germinal center B cells nor MZ B cells were rescued. Additionally, Bcl2 did not rescue the defects in signaling and affinity maturation found in BOB.1/OBF.1-deficient mice. Interestingly, Bcl2-transgenic mice by themselves show an MZ B cell defect. Virtually no functional MZ B cells were detected in these mice. In contrast, mice deficient for Bcl2 show a relative increase in MZ B cell numbers, indicating a previously undetected function of Bcl2 for this B cell compartment.",
publisher = "Rockefeller Univ Press, New York",
journal = "Journal of Experimental Medicine",
title = "B cell-specific transgenic expression of Bcl2 rescues early B lymphopoiesis but not B cell responses in BOB.1/OBF.1-deficient mice",
pages = "1211-1205",
number = "9",
volume = "197",
doi = "10.1084/jem.20022014"
}

Brunner, C., Marinković, D., Klein, J., Samardžić, T., Nitschke, L.,& Wirth, T.. (2003). B cell-specific transgenic expression of Bcl2 rescues early B lymphopoiesis but not B cell responses in BOB.1/OBF.1-deficient mice. in Journal of Experimental Medicine
Rockefeller Univ Press, New York., 197(9), 1205-1211.
https://doi.org/10.1084/jem.20022014

Brunner C, Marinković D, Klein J, Samardžić T, Nitschke L, Wirth T. B cell-specific transgenic expression of Bcl2 rescues early B lymphopoiesis but not B cell responses in BOB.1/OBF.1-deficient mice. in Journal of Experimental Medicine. 2003;197(9):1205-1211.
doi:10.1084/jem.20022014 .

Brunner, C, Marinković, Dragan, Klein, J, Samardžić, T., Nitschke, L., Wirth, Thomas, "B cell-specific transgenic expression of Bcl2 rescues early B lymphopoiesis but not B cell responses in BOB.1/OBF.1-deficient mice" in Journal of Experimental Medicine, 197, no. 9 (2003):1205-1211,
https://doi.org/10.1084/jem.20022014 . .

TY  - JOUR
AU  - Samardžić, T.
AU  - Marinković, Dragan
AU  - Danzer, CP
AU  - Gerlach, J
AU  - Nitschke, L.
AU  - Wirth, Thomas
PY  - 2002
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/30
AB  - CD22 is a B cell-specific member of the immunoglobulin superfamily and binds to sialic acid. CD22 inhibits B cell receptor signaling. Mice deficient for CD22 show a largely normal B cell development. Here, we have performed a detailed analysis of the splenic B cell population and found that the subset of marginal zone (MZ) B cells was selectively reduced in CD22-deficient mice. CD22-deficient mice showed a lack of TNP-ficoll capturing cells in the MZ and a reduced response to TNP-ficoll, particularly when the antigen was applied intravenously. CD22-deficient B cells showed both enhanced motility as well as enhanced chemotaxis to certain chemokines. The altered chemokine responsiveness or the higher signaling capacity of CD22-deficient B cells may lead to the compromised MZ B cell compartment, as both processes have previously been shown to affect MZ composition.
PB  - Wiley-V C H Verlag Gmbh, Weinheim
T2  - European Journal of Immunology
T1  - Reduction of marginal zone B cells in CD22-deficient mice
EP  - 567
IS  - 2
SP  - 561
VL  - 32
DO  - 10.1002/1521-4141(200202)32:2<561::AID-IMMU561>3.0.CO;2-H
ER  - 

@article{
author = "Samardžić, T. and Marinković, Dragan and Danzer, CP and Gerlach, J and Nitschke, L. and Wirth, Thomas",
year = "2002",
abstract = "CD22 is a B cell-specific member of the immunoglobulin superfamily and binds to sialic acid. CD22 inhibits B cell receptor signaling. Mice deficient for CD22 show a largely normal B cell development. Here, we have performed a detailed analysis of the splenic B cell population and found that the subset of marginal zone (MZ) B cells was selectively reduced in CD22-deficient mice. CD22-deficient mice showed a lack of TNP-ficoll capturing cells in the MZ and a reduced response to TNP-ficoll, particularly when the antigen was applied intravenously. CD22-deficient B cells showed both enhanced motility as well as enhanced chemotaxis to certain chemokines. The altered chemokine responsiveness or the higher signaling capacity of CD22-deficient B cells may lead to the compromised MZ B cell compartment, as both processes have previously been shown to affect MZ composition.",
publisher = "Wiley-V C H Verlag Gmbh, Weinheim",
journal = "European Journal of Immunology",
title = "Reduction of marginal zone B cells in CD22-deficient mice",
pages = "567-561",
number = "2",
volume = "32",
doi = "10.1002/1521-4141(200202)32:2<561::AID-IMMU561>3.0.CO;2-H"
}

Samardžić, T., Marinković, D., Danzer, C., Gerlach, J., Nitschke, L.,& Wirth, T.. (2002). Reduction of marginal zone B cells in CD22-deficient mice. in European Journal of Immunology
Wiley-V C H Verlag Gmbh, Weinheim., 32(2), 561-567.
https://doi.org/10.1002/1521-4141(200202)32:2<561::AID-IMMU561>3.0.CO;2-H

Samardžić T, Marinković D, Danzer C, Gerlach J, Nitschke L, Wirth T. Reduction of marginal zone B cells in CD22-deficient mice. in European Journal of Immunology. 2002;32(2):561-567.
doi:10.1002/1521-4141(200202)32:2<561::AID-IMMU561>3.0.CO;2-H .

Samardžić, T., Marinković, Dragan, Danzer, CP, Gerlach, J, Nitschke, L., Wirth, Thomas, "Reduction of marginal zone B cells in CD22-deficient mice" in European Journal of Immunology, 32, no. 2 (2002):561-567,
https://doi.org/10.1002/1521-4141(200202)32:2<561::AID-IMMU561>3.0.CO;2-H . .

TY  - JOUR
AU  - Samardžić, T.
AU  - Gerlach, J
AU  - Muller, K
AU  - Marinković, Dragan
AU  - Hess, J
AU  - Nitschke, L.
AU  - Wirth, Thomas
PY  - 2002
UR  - http://rfasper.fasper.bg.ac.rs/handle/123456789/29
AB  - BOB.1/OBF1 (also called OCA-B), a B lymphocyte-specific transcriptional coactivator, is recruited to octamer-containing promoters by interacting with the Oct-1 or Oct-2 proteins. BOB.1/OBF.1-deficient mice show impaired secondary immunoglobulin isotype secretion and complete absence of germinal centers. Furthermore, numbers of splenic B cells are reduced due to a developmental block at the transitional B cell stage in the bone marrow. We found that surface expression of CD22 is selectively increased on B lineage cells in the bone marrow of BOB.1/OBF.1-deficient mice. CD22 is known as a negative regulator of B cell receptor signaling. We therefore investigated whether defects in B cell development in the BOB.1/OBF1-deficient mice might be due to CD22 up-regulation. Mice were generated lacking both genes. In BOB.1/OBF.1 xCD22 double-deficient mice, numbers of transitional B cells in the bone marrow were normal. Consequently, double-deficient mice also had normal B to T cell ratios in the spleen. We show that BOB.1/OBF.1(-/-) B cells were incapable to induce BCR-triggered Ca2+ mobilization. This Ca2+-signalling defect was restored in BOBA/ OBF1 xCD22 double-deficient B cells. Nevertheless, double-deficient animals were unable to mount humoral immune responses and to form germinal centers. Finally, we demonstrate that CD22(-/-) splenic B cells proliferate independently of BOB.1/OBF1 upon stimulation with LPS. These studies suggest that the B cell differentiation defect observed in BOB.1/OBF.1(-/-) mice is BCR-signal dependent. However, the impairment in germinal center formation is caused by a different mechanism.
PB  - Wiley-V C H Verlag Gmbh, Weinheim
T2  - European Journal of Immunology
T1  - CD22 regulates early B cell development in BOB.1/OBF.1-deficient mice
EP  - 2489
IS  - 9
SP  - 2481
VL  - 32
DO  - 10.1002/1521-4141(200209)32:9_2481::AID-IMMU2481>3.0.CO;2-C
ER  - 

@article{
author = "Samardžić, T. and Gerlach, J and Muller, K and Marinković, Dragan and Hess, J and Nitschke, L. and Wirth, Thomas",
year = "2002",
abstract = "BOB.1/OBF1 (also called OCA-B), a B lymphocyte-specific transcriptional coactivator, is recruited to octamer-containing promoters by interacting with the Oct-1 or Oct-2 proteins. BOB.1/OBF.1-deficient mice show impaired secondary immunoglobulin isotype secretion and complete absence of germinal centers. Furthermore, numbers of splenic B cells are reduced due to a developmental block at the transitional B cell stage in the bone marrow. We found that surface expression of CD22 is selectively increased on B lineage cells in the bone marrow of BOB.1/OBF.1-deficient mice. CD22 is known as a negative regulator of B cell receptor signaling. We therefore investigated whether defects in B cell development in the BOB.1/OBF1-deficient mice might be due to CD22 up-regulation. Mice were generated lacking both genes. In BOB.1/OBF.1 xCD22 double-deficient mice, numbers of transitional B cells in the bone marrow were normal. Consequently, double-deficient mice also had normal B to T cell ratios in the spleen. We show that BOB.1/OBF.1(-/-) B cells were incapable to induce BCR-triggered Ca2+ mobilization. This Ca2+-signalling defect was restored in BOBA/ OBF1 xCD22 double-deficient B cells. Nevertheless, double-deficient animals were unable to mount humoral immune responses and to form germinal centers. Finally, we demonstrate that CD22(-/-) splenic B cells proliferate independently of BOB.1/OBF1 upon stimulation with LPS. These studies suggest that the B cell differentiation defect observed in BOB.1/OBF.1(-/-) mice is BCR-signal dependent. However, the impairment in germinal center formation is caused by a different mechanism.",
publisher = "Wiley-V C H Verlag Gmbh, Weinheim",
journal = "European Journal of Immunology",
title = "CD22 regulates early B cell development in BOB.1/OBF.1-deficient mice",
pages = "2489-2481",
number = "9",
volume = "32",
doi = "10.1002/1521-4141(200209)32:9_2481::AID-IMMU2481>3.0.CO;2-C"
}

Samardžić, T., Gerlach, J., Muller, K., Marinković, D., Hess, J., Nitschke, L.,& Wirth, T.. (2002). CD22 regulates early B cell development in BOB.1/OBF.1-deficient mice. in European Journal of Immunology
Wiley-V C H Verlag Gmbh, Weinheim., 32(9), 2481-2489.
https://doi.org/10.1002/1521-4141(200209)32:9_2481::AID-IMMU2481>3.0.CO;2-C

Samardžić T, Gerlach J, Muller K, Marinković D, Hess J, Nitschke L, Wirth T. CD22 regulates early B cell development in BOB.1/OBF.1-deficient mice. in European Journal of Immunology. 2002;32(9):2481-2489.
doi:10.1002/1521-4141(200209)32:9_2481::AID-IMMU2481>3.0.CO;2-C .

Samardžić, T., Gerlach, J, Muller, K, Marinković, Dragan, Hess, J, Nitschke, L., Wirth, Thomas, "CD22 regulates early B cell development in BOB.1/OBF.1-deficient mice" in European Journal of Immunology, 32, no. 9 (2002):2481-2489,
https://doi.org/10.1002/1521-4141(200209)32:9_2481::AID-IMMU2481>3.0.CO;2-C . .

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 . .