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 . .