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International Immunology Advance Access originally published online on December 21, 2007
International Immunology 2008 20(2):165-175; doi:10.1093/intimm/dxm133
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© The Japanese Society for Immunology. 2007. All rights reserved. For permissions, please e-mail: journals.permissions@oxfordjournals.org

Selective silencing of disease-associated B-lymphocytes by chimeric molecules targeting their Fc{gamma}IIb receptor

Nikolina Mihaylova1, Elisaveta Voynova1, Andrey Tchorbanov1, Maria Nikolova2, Antoaneta Michova2, Todor Todorov3, Luba Srebreva4, Hristo Taskov2 and Tchavdar Vassilev1

1 Department of Immunology, Institute of Microbiology, Bulgarian Academy of Sciences, Sofia, Bulgaria
2 Central Laboratory of Immunology, National Center of Infectious and Parasitic Diseases, Sofia, Bulgaria
3 Department of Pathology, Sofia Medical School, Sofia, Bulgaria
4 Department of Gene Regulation, Institute of Molecular Biology, Bulgarian Academy of Sciences, Sofia, Bulgaria

Correspondence to: T. Vassilev, Stefan Angelov Institute of Microbiology, Academy G. Bonchev Street, Block 26, 1113 Sofia, Bulgaria. E-mail: vassilev{at}microbio.bas.bg

The presently used approaches to silence autoreactive disease-associated B cells act indiscriminately and more specific therapies are obviously needed. In the present study, we analyze the ability of a chimeric antibody to suppress selectively pathological autoreactive B-lymphocytes in lupus-prone mice by cross-linking their surface Ig receptors with the inhibitory IgG Fc{gamma}RIIb receptors. The chimera was constructed by coupling an immunodominant mouse Histone 1 peptide to a rat monoclonal anti-mouse CD32 (Fc{gamma}RIIb) antibody. The administration of these chimeric molecules to MRL/lpr mice with initial and with full-blown disease resulted in the reduction of the levels of IgG anti-Histone 1 antibodies, of the albuminuria levels, of the size of lymphoid organs and in prevention of the development of skin lesions. The observed effect was limited to lupus-associated B cells only, as the treatment did not decrease the IgG antibody response to an administered foreign antigen. This study demonstrates the possibility to silence selectively autoreactive B cells and to delay the progression of an autoimmune disease using chimeric antibody molecules.

Keywords: auto-antibodies, Fc{gamma}RIIb, Histone 1, lupus

Transmitting editor: S. Izui

Received 6 July 2006, accepted 5 November 2007.


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