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CD22 and CD72 are inhibitory receptors dominantly expressed in B lymphocytes and regulate systemic autoimmune diseases

English version

CD22 und CD72 sind in B-Lymphozyten dominant exprimierte inhibitorische Rezeptoren und regulieren systemische Autoimmunerkrankungen

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References

  1. Tsubata T (2012) Role of inhibitory BCR co-receptors in immunity. Infect Disord Drug Targets 12:181–190

    Article  CAS  PubMed  Google Scholar 

  2. Niederer HA, Clatworthy MR, Willcocks LC, Smith KG (2010) FcgammaRIIB, FcgammaRIIIB, and systemic lupus erythematosus. Ann N Y Acad Sci 1183:69–88

    Article  CAS  PubMed  Google Scholar 

  3. Hennet T, Chui D, Paulson JC, Marth JD (1998) Immune regulation by the ST6Gal sialyltransferase. Proc Natl Acad Sci U S A 95:4504–4509

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  4. Collins BE, Smith BA, Bengtson P, Paulson JC (2006) Ablation of CD22 in ligand-deficient mice restores B cell receptor signaling. Nat Immunol 7:199–206

    Article  CAS  PubMed  Google Scholar 

  5. Ghosh S, Bandulet C, Nitschke L (2006) Regulation of B cell development and B cell signalling by CD22 and its ligands alpha2,6-linked sialic acids. Int Immunol 18:603–611

    Article  CAS  PubMed  Google Scholar 

  6. Jin L (2002) Sialic Acid binding domains of CD22 are required for negative regulation of B cell receptor signaling. J Exp Med 195:1199–1205

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  7. Muller J, Obermeier I, Wohner M et al (2013) CD22 ligand-binding and signaling domains reciprocally regulate B-cell Ca2+ signaling. Proc Natl Acad Sci U S A 110:12402–12407

    Article  PubMed  PubMed Central  Google Scholar 

  8. Poe JC, Fujimoto Y, Hasegawa M et al (2004) CD22 regulates B lymphocyte function in vivo through both ligand-dependent and ligand-independent mechanisms. Nat Immunol 5:1078–1087

    Article  CAS  PubMed  Google Scholar 

  9. Macauley MS, Crocker PR, Paulson JC (2014) Siglec-mediated regulation of immune cell function in disease. Nat Rev Immunol 14:653–666

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  10. Carlin AF, Uchiyama S, Chang YC et al (2009) Molecular mimicry of host sialylated glycans allows a bacterial pathogen to engage neutrophil Siglec-9 and dampen the innate immune response. Blood 113:3333–3336

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  11. Chang YC, Olson J, Beasley FC et al (2014) Group B Streptococcus engages an inhibitory Siglec through sialic acid mimicry to blunt innate immune and inflammatory responses in vivo. PLoS Pathog 10:e1003846

    Article  PubMed  PubMed Central  Google Scholar 

  12. Erdmann H, Steeg C, Koch-Nolte F et al (2009) Sialylated ligands on pathogenic Trypanosoma cruzi interact with Siglec-E (sialic acid-binding Ig-like lectin-E). Cell Microbiol 11:1600–1611

    Article  CAS  PubMed  Google Scholar 

  13. Hutzler S, Ozgor L, Naito-Matsui Y et al (2014) The ligand-binding domain of Siglec-G is crucial for its selective inhibitory function on B1 cells. J Immunol 192:5406–5414

    Article  CAS  PubMed  Google Scholar 

  14. Jellusova J, Wellmann U, Amann K et al (2010) CD22 x Siglec-G double-deficient mice have massively increased B1 cell numbers and develop systemic autoimmunity. J Immunol 184:3618–3627

    Article  CAS  PubMed  Google Scholar 

  15. Oishi H, Tsubaki T, Miyazaki T et al (2013) A bacterial artificial chromosome transgene with polymorphic Cd72 inhibits the development of glomerulonephritis and vasculitis in MRL-Faslpr lupus mice. J Immunol 190:2129–2137

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  16. Xu M, Hou R, Sato-Hayashizaki A et al (2013) Cd72(c) is a modifier gene that regulates Fas(lpr)-induced autoimmune disease. J Immunol 190:5436–5445

    Article  CAS  PubMed  Google Scholar 

  17. Li DH, Winslow MM, Cao TM et al (2008) Modulation of peripheral B cell tolerance by CD72 in a murine model. Arthritis Rheum 58:3192–3204

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  18. Hitomi Y, Tsuchiya N, Kawasaki A et al (2004) CD72 polymorphisms associated with alternative splicing modify susceptibility to human systemic lupus erythematosus through epistatic interaction with FCGR2B. Hum Mol Genet 13:2907–2917

    Article  CAS  PubMed  Google Scholar 

  19. Xu J, Lu S, Tao J et al (2008) CD72 polymorphism associated with child-onset of idiopathic thrombocytopenic purpura in Chinese patients. J Clin Immunol 28:214–219

    Article  CAS  PubMed  Google Scholar 

  20. Van de Velde H, Hoegen I von, Luo W et al (1991) The B-cell surface protein CD72/Lyb-2 is the ligand for CD5. Nature 351:662–665

    Article  Google Scholar 

  21. Kumanogoh A, Watanabe C, Lee I et al (2000) Identification of CD72 as a lymphocyte receptor for the class IV semaphorin CD100: a novel mechanism for regulating B cell signaling. Immunity 13:621–631

    Article  CAS  PubMed  Google Scholar 

  22. Daridon C, Blassfeld D, Reiter K et al (2010) Epratuzumab targeting of CD22 affects adhesion molecule expression and migration of B-cells in systemic lupus erythematosus. Arthritis Res Ther 12:R204

    Article  PubMed  PubMed Central  Google Scholar 

  23. Rossi EA, Goldenberg DM, Michel R et al (2013) Trogocytosis of multiple B-cell surface markers by CD22 targeting with epratuzumab. Blood 122:3020–3029

    Article  CAS  PubMed  Google Scholar 

  24. Sieger N, Fleischer SJ, Mei HE et al (2013) CD22 ligation inhibits downstream B cell receptor signaling and Ca(2+) flux upon activation. Arthritis Rheum 65:770–779

    Article  CAS  PubMed  Google Scholar 

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Compliance with ethical guidelines

Conflict of interest. T. Tsubata states that there are no conflicts of interest.

The accompanying manuscript does not include studies on humans or animals.

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  1. Department of Immunology, Medical Research Institute, Tokyo Medical and Dental University, 1–5–45 Yushima, 113–8510, Bunkyo-ku, Tokyo, Japan

    T. Tsubata

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  1. T. Tsubata
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Correspondence to T. Tsubata.

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This article is the English version of “CD22 und CD72 sind in B-Lymphozyten dominant exprimierte inhibitorische Rezeptoren und regulieren systemische Autoimmunerkrankungen”, DOI 10.1007/s00393-015-0038-2.

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Tsubata, T. CD22 and CD72 are inhibitory receptors dominantly expressed in B lymphocytes and regulate systemic autoimmune diseases. Z Rheumatol 76 (Suppl 1), 10–13 (2017). https://doi.org/10.1007/s00393-015-1577-2

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  • DOI: https://doi.org/10.1007/s00393-015-1577-2

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