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Identification and Characterization of a Human CD5⁺ Pre-Naive B Cell Population¹

Jisoo Lee^*,, Stefan Kuchen, Randy Fischer, Sooghee Chang and Peter E. Lipsky^2,

^* Division of Rheumatology, Department of Internal Medicine, Ewha Womans University School of Medicine, Seoul, Korea; Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892; and Rheumatism Research Center, Catholic University College of Medicine, Seoul, Korea

We have identified a distinct pre-naive B cell population circulating in human peripheral blood that exhibits an intermediate phenotype between transitional and naive B cells. Like human transitional B cells, these cells express CD5 but have intermediate densities of CD38, CD10, CD9, and the ABCB1 transporter compared with transitional and naive B cells. These pre-naive B cells account for a majority of circulating human CD5⁺ B cells. Importantly, CD5⁺ pre-naive B cells could be induced to differentiate into cells with a naive phenotype in vitro. CD5⁺ pre-naive B cells show only partial responses to BCR stimulation and CD40 ligation and undergo more spontaneous apoptosis and cell death than do naive B cells, whereas BAFF/BLyS (B cell-activating factor belonging to the TNF family) did not enhance their survival compared with naive B cells. In contrast, CD5⁺ pre-naive B cells carry out certain functions comparable to naive B cells, including the capacity to differentiate into plasma cells and the ability to function as APCs. Notably, an increased proportion of CD5⁺ pre-naive B cells were found in peripheral blood of patients with systemic lupus erythematosus. These results have identified a unique intermediate in human naive B cell development within the peripheral blood and derangements of its homeostasis in patients with systemic lupus erythematosus.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This research was supported in part by the National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health. J.L. was supported by the Korea Research Foundation Grant KRF-2005-331-E00123. S.K. was supported by the Jean et Linette Warnery Foundation and the Swiss Foundation for Medical-Biological Scholarships.

² Address correspondence and reprint requests to Dr. Peter E. Lipsky, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Building 10, Room 6D47C, Bethesda, MD 20892. E-mail address: peterlipsky{at}comcast.net

³ Abbreviations used in this paper: SLE, systemic lupus erythematosus; BAFF/BlyS, B cell-activating factor belonging to the TNF family.