Hase Hidenori, Kanno Yumiko, Kojima Masaru, Hasegawa Kaoru, Sakurai Daisuke, Kojima Hidefumi, Tsuchiya Naoyuki, Tokunaga Katsushi, Masawa Nobuhide, Azuma Miyuki, Okumura Ko, Kobata Tetsuji
Division of Immunology, Institute for Medical Science, and Department of Pathology, Dokkyo University School of Medicine, Mibu, Tochigi 321-0293, Japan
Blood. 2004 Mar 15;103(6):2257-65. doi: 10.1182/blood-2003-08-2694. Epub 2003 Nov 20.
The tumor necrosis factor (TNF)-like ligand BAFF/BLyS (B-cell activating factor of the TNF family/B-lymphocyte stimulator) is a potent B-cell survival factor, yet its functional relationship with other B-cell surface molecules such as CD19 and CD40 is poorly understood. We found that follicular dendritic cells (FDCs) in human lymph nodes expressed BAFF abundantly. BAFF up-regulated a B cell-specific transcription factor Pax5/BSAP (Pax5/B cell-specific activator protein) activity and its target CD19, a major component of the B-cell coreceptor complex, and synergistically enhanced CD19 phosphorylation by B-cell antigen receptor (BCR). BAFF further enhanced B-cell proliferation, immunoglobulin G (IgG) production, and reactivity to CD154 by BCR/CD19 coligation and interleukin-15 (IL-15). Our results suggest that BAFF may play an important role in FDC-B-cell interactions through the B-cell coreceptor complex and a possibly sequential link between the T cell-independent and -dependent B-cell responses in the germinal centers.
肿瘤坏死因子（TNF）样配体BAFF/BLyS（TNF家族的B细胞活化因子/ B淋巴细胞刺激因子）是一种有效的B细胞存活因子，但其与其他B细胞表面分子（如CD19和CD40）的功能关系仍知之甚少。我们发现人淋巴结中的滤泡树突状细胞（FDC）大量表达BAFF。BAFF上调了B细胞特异性转录因子Pax5/BSAP（Pax5/ B细胞特异性激活蛋白）的活性及其靶标CD19（B细胞共受体复合物的主要成分），并协同增强了B细胞抗原受体（BCR）介导的CD19磷酸化。BAFF通过BCR/CD19共连接和白细胞介素-15（IL-15）进一步增强了B细胞增殖、免疫球蛋白G（IgG）产生以及对CD154的反应性。我们的结果表明，BAFF可能通过B细胞共受体复合物在FDC-B细胞相互作用中发挥重要作用，并且可能在生发中心T细胞非依赖性和依赖性B细胞反应之间存在顺序联系。
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