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B cell antigen receptor-evoked calcium influx is enhanced in CD22-deficient B cell lines.
J Immunol. 1997 Nov 01; 159(9):4233-43.JI

Abstract

CD22 is a B cell membrane glycoprotein that, upon Ag receptor engagement, becomes rapidly tyrosyl phosphorylated and associates with several signaling molecules including Lyn, Syk, PLCgamma1, and the protein-tyrosine phosphatase, SHP-1. Two allelic forms of murine CD22 exist: CD22.1 is expressed in strains such as NZB and DBA/2, whereas CD22.2 is expressed in BALB/c and most other strains. WEHI-231 cells, which derive from a (BALB/c x NZB)F1 mouse, express one copy of each allele. Previous studies have proposed both positive and negative functions for CD22. We explored the role of CD22 in surface IgM Ag receptor signal transduction by examining signaling in three clonally independent WEHI-231 variants that have lost expression of the CD22.2 allele. This experimental design allowed us to assess the signaling functions of CD22 independent of its developmental role. These variants, which exhibit a 50% reduction of total surface CD22, are hyper-responsive to Ag receptor stimulation: several cellular proteins are hyperphosphorylated on tyrosyl residues and surface IgM-mediated calcium flux is markedly increased. Interestingly, the increased calcium response observed in CD22-deficient cells is due largely to enhanced calcium influx. Reconstitution of CD22 expression reduces these changes. The SHP-1/CD22 association is reduced in CD22-deficient cell lines and is restored by re-expression of CD22. Our results demonstrate that CD22 is a cell autonomous negative regulator of B cell Ag receptor signaling, and suggest that it regulates calcium entry via a mechanism downstream from or independent of calcium release from intracellular stores.

Authors+Show Affiliations

Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

9379018

Citation

Nadler, M J., et al. "B Cell Antigen Receptor-evoked Calcium Influx Is Enhanced in CD22-deficient B Cell Lines." Journal of Immunology (Baltimore, Md. : 1950), vol. 159, no. 9, 1997, pp. 4233-43.
Nadler MJ, McLean PA, Neel BG, et al. B cell antigen receptor-evoked calcium influx is enhanced in CD22-deficient B cell lines. J Immunol. 1997;159(9):4233-43.
Nadler, M. J., McLean, P. A., Neel, B. G., & Wortis, H. H. (1997). B cell antigen receptor-evoked calcium influx is enhanced in CD22-deficient B cell lines. Journal of Immunology (Baltimore, Md. : 1950), 159(9), 4233-43.
Nadler MJ, et al. B Cell Antigen Receptor-evoked Calcium Influx Is Enhanced in CD22-deficient B Cell Lines. J Immunol. 1997 Nov 1;159(9):4233-43. PubMed PMID: 9379018.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - B cell antigen receptor-evoked calcium influx is enhanced in CD22-deficient B cell lines. AU - Nadler,M J, AU - McLean,P A, AU - Neel,B G, AU - Wortis,H H, PY - 1997/10/31/pubmed PY - 1997/10/31/medline PY - 1997/10/31/entrez SP - 4233 EP - 43 JF - Journal of immunology (Baltimore, Md. : 1950) JO - J Immunol VL - 159 IS - 9 N2 - CD22 is a B cell membrane glycoprotein that, upon Ag receptor engagement, becomes rapidly tyrosyl phosphorylated and associates with several signaling molecules including Lyn, Syk, PLCgamma1, and the protein-tyrosine phosphatase, SHP-1. Two allelic forms of murine CD22 exist: CD22.1 is expressed in strains such as NZB and DBA/2, whereas CD22.2 is expressed in BALB/c and most other strains. WEHI-231 cells, which derive from a (BALB/c x NZB)F1 mouse, express one copy of each allele. Previous studies have proposed both positive and negative functions for CD22. We explored the role of CD22 in surface IgM Ag receptor signal transduction by examining signaling in three clonally independent WEHI-231 variants that have lost expression of the CD22.2 allele. This experimental design allowed us to assess the signaling functions of CD22 independent of its developmental role. These variants, which exhibit a 50% reduction of total surface CD22, are hyper-responsive to Ag receptor stimulation: several cellular proteins are hyperphosphorylated on tyrosyl residues and surface IgM-mediated calcium flux is markedly increased. Interestingly, the increased calcium response observed in CD22-deficient cells is due largely to enhanced calcium influx. Reconstitution of CD22 expression reduces these changes. The SHP-1/CD22 association is reduced in CD22-deficient cell lines and is restored by re-expression of CD22. Our results demonstrate that CD22 is a cell autonomous negative regulator of B cell Ag receptor signaling, and suggest that it regulates calcium entry via a mechanism downstream from or independent of calcium release from intracellular stores. SN - 0022-1767 UR - https://www.unboundmedicine.com/medline/citation/9379018/B_cell_antigen_receptor_evoked_calcium_influx_is_enhanced_in_CD22_deficient_B_cell_lines_ L2 - https://www.jimmunol.org/lookup/pmidlookup?view=long&pmid=9379018 DB - PRIME DP - Unbound Medicine ER -