RESEARCH - Peripheral B cell abnormalities in patients with SLE in a quiescent phase

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J Autoimmun. 2009 Dec 4. [Epub ahead of print]

Peripheral B cell abnormalities in patients with systemic lupus

erythematosus in quiescent phase: Decreased memory B cells and

membrane CD19 expression.

Korganow AS, Knapp AM, Nehme-Schuster H, Soulas-Sprauel P, Poindron V,

Pasquali JL, T.

CNRS UPR9021, Université de Strasbourg (UDS), Hopitaux Universitaires

de Strasbourg, Strasbourg, France.

B lymphocytes from patients with systemic lupus erythematosus (SLE)

are hyperactive and produce autoantibodies. Several B cell phenotype

characteristics such as the expansion of activated populations, and of

a newly identified memory compartment have already been reported.

These results are not easy to interpret because of the clinical

heterogeneity of SLE, as well as the difficulties to establish

homogeneous and well defined groups taking in consideration the

activity of the disease and the various therapies. However, although

many mediators and mechanisms can contribute to the clinical

presentation and subsequent progression of individuals with SLE,

several data suggest that some intrinsic B cells abnormalities may be

central to the disease process. In this view, we have analysed the

phenotype of B cells from 18 patients with quiescent diseases (mean

SLEDAI score below 2) and from 11 healthy controls. B cell surface

marker expression was determined by flow cytometry. We analysed the

main B cell sub-populations. We demonstrate the persistence of

plasmocyte-differentiated and -activated B cells even in quiescent

patients. However, quiescent patients display a decrease in memory B

cells that could reflect the control of their disease. Above all, we

describe a lower membrane expression of the CD19 protein on all B

cells in every patient compared to controls. This lower CD19

expression is associated with reduced CD45 levels. It is not

associated with an evident gene expression alteration and in vitro

stimulation restores a control phenotype. These findings suggest

certain mechanisms of lupus development.

PMID: 19963348

http://www.ncbi.nlm.nih.gov/pubmed/19963348

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