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B cell defects in SLP65/BLNK-deficient mice can be partially corrected by the absence of CD22, an inhibitory coreceptor for BCR signaling.
Eur J Immunol. 2003 Dec; 33(12):3418-26.EJ

Abstract

CD22 is an inhibitory coreceptor for B cell receptor (BCR) signaling. The inhibition is most likely mediated by activation of SHP-1. We found that SLP65/BLNK reaches maximal tyrosine-phosphorylation at earlier time points in CD22(-/-) than in wild type B cells upon BCR cross-linking, suggesting that SLP65/BLNK is a substrate of SHP-1. However, in contrast to the defective Ca(2+) mobilization of SLP65/BLNK(-/-) B cells, there was a clear Ca(2+) response in SLP65/BLNKxCD22 double-deficient B cells. This implies that SLP65/BLNK is not the sole target of SHP-1 in the regulation of the Ca(2+) signaling strength. While SLP65(-/-) mice show several blocks of B cell differentiation, in SLP65/BLNK x CD22 double-deficient mice the maturation block of B cells in the spleen was partially rescued. However, the proliferative responses of B cells from both SLP65/BLNK(-/-) and double-deficient mice were defective after IgM- or CD40-stimulation. These results show that SLP65/BLNK is not absolutely essential for Ca(2+) induction in B cells, because the deficiency of this adapter can be by-passed by the additional deletion of an inhibitory receptor. Furthermore, these experiments suggest that B cell maturation in the spleen is directly dependent on the strength of BCR-derived Ca(2+) signals.

Authors+Show Affiliations

Institute for Virology and Immunobiology, University of Würzburg, Würzburg, 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

14635051

Citation

Gerlach, Judith, et al. "B Cell Defects in SLP65/BLNK-deficient Mice Can Be Partially Corrected By the Absence of CD22, an Inhibitory Coreceptor for BCR Signaling." European Journal of Immunology, vol. 33, no. 12, 2003, pp. 3418-26.
Gerlach J, Ghosh S, Jumaa H, et al. B cell defects in SLP65/BLNK-deficient mice can be partially corrected by the absence of CD22, an inhibitory coreceptor for BCR signaling. Eur J Immunol. 2003;33(12):3418-26.
Gerlach, J., Ghosh, S., Jumaa, H., Reth, M., Wienands, J., Chan, A. C., & Nitschke, L. (2003). B cell defects in SLP65/BLNK-deficient mice can be partially corrected by the absence of CD22, an inhibitory coreceptor for BCR signaling. European Journal of Immunology, 33(12), 3418-26.
Gerlach J, et al. B Cell Defects in SLP65/BLNK-deficient Mice Can Be Partially Corrected By the Absence of CD22, an Inhibitory Coreceptor for BCR Signaling. Eur J Immunol. 2003;33(12):3418-26. PubMed PMID: 14635051.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - B cell defects in SLP65/BLNK-deficient mice can be partially corrected by the absence of CD22, an inhibitory coreceptor for BCR signaling. AU - Gerlach,Judith, AU - Ghosh,Snigdha, AU - Jumaa,Hassan, AU - Reth,Michael, AU - Wienands,Jürgen, AU - Chan,Andrew C, AU - Nitschke,Lars, PY - 2003/11/25/pubmed PY - 2004/1/24/medline PY - 2003/11/25/entrez SP - 3418 EP - 26 JF - European journal of immunology JO - Eur J Immunol VL - 33 IS - 12 N2 - CD22 is an inhibitory coreceptor for B cell receptor (BCR) signaling. The inhibition is most likely mediated by activation of SHP-1. We found that SLP65/BLNK reaches maximal tyrosine-phosphorylation at earlier time points in CD22(-/-) than in wild type B cells upon BCR cross-linking, suggesting that SLP65/BLNK is a substrate of SHP-1. However, in contrast to the defective Ca(2+) mobilization of SLP65/BLNK(-/-) B cells, there was a clear Ca(2+) response in SLP65/BLNKxCD22 double-deficient B cells. This implies that SLP65/BLNK is not the sole target of SHP-1 in the regulation of the Ca(2+) signaling strength. While SLP65(-/-) mice show several blocks of B cell differentiation, in SLP65/BLNK x CD22 double-deficient mice the maturation block of B cells in the spleen was partially rescued. However, the proliferative responses of B cells from both SLP65/BLNK(-/-) and double-deficient mice were defective after IgM- or CD40-stimulation. These results show that SLP65/BLNK is not absolutely essential for Ca(2+) induction in B cells, because the deficiency of this adapter can be by-passed by the additional deletion of an inhibitory receptor. Furthermore, these experiments suggest that B cell maturation in the spleen is directly dependent on the strength of BCR-derived Ca(2+) signals. SN - 0014-2980 UR - https://www.unboundmedicine.com/medline/citation/14635051/B_cell_defects_in_SLP65/BLNK_deficient_mice_can_be_partially_corrected_by_the_absence_of_CD22_an_inhibitory_coreceptor_for_BCR_signaling_ L2 - https://doi.org/10.1002/eji.200324290 DB - PRIME DP - Unbound Medicine ER -