This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Schuster, H Articles by Korganow, A S Search for Related Content PubMed PubMed Citation Articles by Schuster, H Articles by Korganow, A S Social Bookmarking                         What's this?

Expansion of marginal zone B cells is not sufficient for the development of renal disease in NZBxNZW F1 mice

T Martin

Laboratoire d'Immunopathologie, Institut d'Hématologie et d'Immunologie, Strasbourg, France

L Marcellin

Service d'Anatomopathologie, Hopital de Hautepierre, Strasbourg, France

J-C Garaud

J-L Pasquali

A S Korganow

Laboratoire d'Immunopathologie, Institut d'Hématologie et d'Immunologie, Strasbourg, France; Institut d'Hématologie et d'Immunologie, 1 place de l'Hopital, 67091 Strasbourg Cedex, FranceAnne-Sophie.Korganow{at}chru-strasbourg.fr

The mechanisms which govern the production of autoantibodies and of tissue damage during systemic lupus (SLE) are still unclear. In the NZB£NZW F1 (BW) model of SLE glomerulonephritis, the activation and commitment of B cells are thought to play a major role in disease progression. Previous analysis has suggested that these mice have a substantial increase of marginal zone (MZ) B cells before the occurrence of the disease. Owing to the probable role of this B cell subset in autoantibody production, it was important to define the possible link between this abnormality and the occurrence of kidney damage.

Using cytofluorometry analysis, we followed the splenic MZ B cell phenotype in different series of mice with shared autoimmune genetic background and histologically defined renal status.

By comparing BW females and BW males, NZB and NZW mice, we confirm that BW mice have an increase in MZ B cells but this MZ B cells expansion is not directly linked to tissue lesions. Genetically modified BW female mice with a restricted repertoire of B and T cell antigen receptors, and which do not develop nephritis, exhibit the same increase of MZ B cells, suggesting that this increase does not depend on a specific set of antigens. Moreover, our analysis brings to light a predisease state in BW males, with autoantibody production and mesangial deposits.

Key Words: marginal zone B cells • lupus • mice (NZB£NZW)F1

Lupus, Vol. 11, No. 5, 277-286 (2002)
DOI: 10.1191/0961203302lu191oa


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				P. A. Silveira, H. D. Chapman, J. Stolp, E. Johnson, S. L. Cox, K. Hunter, L. S. Wicker, and D. V. Serreze Genes within the Idd5 and Idd9/11 Diabetes Susceptibility Loci Affect the Pathogenic Activity of B Cells in Nonobese Diabetic Mice J. Immunol., November 15, 2006; 177(10): 7033 - 7041. [Abstract] [Full Text] [PDF]

				M. Wakui, L. Morel, E. J. Butfiloski, C. Kim, and E. S. Sobel Genetic Dissection of Systemic Lupus Erythematosus Pathogenesis: Partial Functional Complementation between Sle1 and Sle3/5 Demonstrates Requirement for Intracellular Coexpression for Full Phenotypic Expression of Lupus J. Immunol., July 15, 2005; 175(2): 1337 - 1345. [Abstract] [Full Text] [PDF]

				M. K. Haraldsson, N. G. dela Paz, J. G. Kuan, G. S. Gilkeson, A. N. Theofilopoulos, and D. H. Kono Autoimmune Alterations Induced by the New Zealand Black Lbw2 Locus in BWF1 Mice J. Immunol., April 15, 2005; 174(8): 5065 - 5073. [Abstract] [Full Text] [PDF]

				S. Atencio, H. Amano, S. Izui, and B. L. Kotzin Separation of the New Zealand Black Genetic Contribution to Lupus from New Zealand Black Determined Expansions of Marginal Zone B and B1a Cells J. Immunol., April 1, 2004; 172(7): 4159 - 4166. [Abstract] [Full Text] [PDF]

				M. Batten, C. Fletcher, L. G. Ng, J. Groom, J. Wheway, Y. Laabi, X. Xin, P. Schneider, J. Tschopp, C. R. Mackay, et al. TNF Deficiency Fails to Protect BAFF Transgenic Mice against Autoimmunity and Reveals a Predisposition to B Cell Lymphoma J. Immunol., January 15, 2004; 172(2): 812 - 822. [Abstract] [Full Text] [PDF]