Peripheral B cell abnormalities in patients with systemic lupus erythematosus in quiescent phase: Decreased memory B cells and membrane CD19 expression

详细信息    查看全文

• 作者：Anne-Sophie Korganow ; Anne-Marie Knapp ; Hé ; lè ; ne Nehme-Schuster ; Pauline Soulas-Sprauel ; Vincent Poindron ; Jean-Louis Pasquali ; Thierry Martin
• 关键词：Systemic lupus erythematosus (SLE) ; Quiescent lupus patients ; Peripheral B cells ; Memory B cells ; CD19 expression
• 刊名：Journal of Autoimmunity
• 出版年：2010
• 出版时间：June 2010
• 年：2010
• 卷：34
• 期：4
• 页码：426-434
• 全文大小：341 K

文摘

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.