Sims, G. P. et al. Identification and characterization of circulating human transitional B cells. Blood 105, 4390-4398

Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institute of Health, Bethesda, MD, USA.
Blood (Impact Factor: 10.45). 07/2005; 105(11):4390-8. DOI: 10.1182/blood-2004-11-4284
Source: PubMed


Murine B-cell development begins in bone marrow and results in the generation of immature transitional B cells that transit to the spleen to complete their maturation. It remains unclear whether the same developmental pathway takes place in humans. Using markers characteristic of human bone marrow immature B cells, we have identified a population of circulating human B cells with a phenotype most similar to mouse transitional type I (T1) B cells, although these human counterparts express CD5. These cells die rapidly in culture, and B-cell activation factor member of the tumor necrosis factor (TNF) family (BAFF) does not effect their survival regardless of B-cell receptor (BCR) stimulation. In contrast, bone marrow stromal cells or interleukin-4 (IL-4) significantly enhanced their survival. In the presence of T-cell signals provided by IL-4 or CD40 ligation, BCR stimulation can induce progression into cell cycle. Interestingly, circulating B cells that phenotypically and functionally resemble murine T2 B cells are found in cord blood and adult peripheral blood, suggesting that B-cell maturation may not be restricted to the spleen. Notably, increased proportions of T1 B cells were found in blood of patients with systemic lupus erythematosus (SLE), although bone marrow production and selection appeared to be normal.

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Available from: Gary Sims, Mar 13, 2014
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    • "The existence of B10 in humans remains unclear and is currently difficult to unify in a coherent model (Table 1). An orthologous IL-10-producing B cell has been described in the CD24highCD38high transitional B cell subset (23, 59). Interestingly, this population displays regulatory capacities in healthy volunteers, manifested by the suppression of the Th1 cell differentiation that appears deficient in systemic lupus erythematosus (SLE) patients. "
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    • "Consistently, our data allow us to exclude that the expansion of transitional B cells is due to homeostatic proliferation since we demonstrated the absence of replication history in this subset. Transitional B cells are found expanded in immunodeficient conditions [40] or autoimmune diseases [41] and represent a reservoir of autoreactive B cells [42]. The cohort of patients analyzed here did not show any overt sign of autoimmunity, probably due to their young age. "
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