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*
Istituto Ricerche Farmacologiche "Mario Negri,"
Fondazione Matarelli, Hospital Fatebenefratelli e Oftalmico, and
Department of Pathological Anatomy, Hospital L. Sacco, Milan, Italy;
§
Department of Hematology, University College London Medical School, London, United Kingdom; and
¶
Department of Experimental Oncology A, Istituto Nazionale dei Tumori, Milan, and
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Department of Experimental Medicine and Pathology, Immunopathology Section, Università di Roma La Sapienza, Rome, Italy
The A-Myb transcription factor is structurally related to the
c-myb proto-oncogene and is involved in the control of
proliferation and/or differentiation of mature B lymphocytes. We have
shown previously by PCR analysis that A-myb is
preferentially expressed in
CD38+CD39-sIgM- mature B cells.
We demonstrate here, using in situ hybridization, that A-mybexpression is restricted to the dark zone of human tonsils and
lymph nodes. Furthermore, we show that A-Myb expression is cell cycle
regulated both in tonsillar B cells and in Burkitt’s lymphoma cell
lines, being detectable only in the S and G2/M phases of
the cell cycle and not in G0/G1 phase. Strong
proliferation of resting human B cells induced in vitro by a variety of
physiologic signals, including anti-µ, CD40 ligand, IL-2, IL-4,
IL-6, IL-13, IFN-
, TNF-
, anti-CD19, and anti-CD20, failed
to induce A-myb expression, suggesting that proliferation
alone is not sufficient for A-myb expression in the absence
of induction of a true centroblast phenotype. Finally, we show that
differentiation of germinal center B cells in vitro toward either
memory or plasma cells is accompanied by rapid down-regulation of
A-myb expression. We conclude that A-myb is a
marker of centroblasts generated in vivo.
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