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CD22 regulates early B cell development in BOB.1/OBF.1-deficient mice.
Eur J Immunol. 2002 Sep; 32(9):2481-9.EJ

Abstract

BOB.1/OBF.1 (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/OBF.1-deficient mice might be due to CD22 up-regulation. Mice were generated lacking both genes. In BOB.1/OBF.1xCD22 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 Ca(2+) mobilization. This Ca(2+)-signalling defect was restored in BOB.1/OBF.1xCD22 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/OBF.1 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.

Authors+Show Affiliations

Department of Physiological Chemistry, Ulm University, Germany.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12207332

Citation

Samardzic, Tatjana, et al. "CD22 Regulates Early B Cell Development in BOB.1/OBF.1-deficient Mice." European Journal of Immunology, vol. 32, no. 9, 2002, pp. 2481-9.
Samardzic T, Gerlach J, Muller K, et al. CD22 regulates early B cell development in BOB.1/OBF.1-deficient mice. Eur J Immunol. 2002;32(9):2481-9.
Samardzic, T., Gerlach, J., Muller, K., Marinkovic, D., Hess, J., Nitschke, L., & Wirth, T. (2002). CD22 regulates early B cell development in BOB.1/OBF.1-deficient mice. European Journal of Immunology, 32(9), 2481-9.
Samardzic T, et al. CD22 Regulates Early B Cell Development in BOB.1/OBF.1-deficient Mice. Eur J Immunol. 2002;32(9):2481-9. PubMed PMID: 12207332.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - CD22 regulates early B cell development in BOB.1/OBF.1-deficient mice. AU - Samardzic,Tatjana, AU - Gerlach,Judith, AU - Muller,Kerstin, AU - Marinkovic,Dragan, AU - Hess,Jochen, AU - Nitschke,Lars, AU - Wirth,Thomas, PY - 2002/9/11/pubmed PY - 2002/11/26/medline PY - 2002/9/11/entrez SP - 2481 EP - 9 JF - European journal of immunology JO - Eur J Immunol VL - 32 IS - 9 N2 - BOB.1/OBF.1 (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/OBF.1-deficient mice might be due to CD22 up-regulation. Mice were generated lacking both genes. In BOB.1/OBF.1xCD22 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 Ca(2+) mobilization. This Ca(2+)-signalling defect was restored in BOB.1/OBF.1xCD22 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/OBF.1 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. SN - 0014-2980 UR - https://www.unboundmedicine.com/medline/citation/12207332/CD22_regulates_early_B_cell_development_in_BOB_1/OBF_1_deficient_mice_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0014-2980&date=2002&volume=32&issue=9&spage=2481 DB - PRIME DP - Unbound Medicine ER -