Macrophage-derived BAFF induces AID expression through the p38MAPK/CREB and JNK/AP-1 pathways

Journal of Leukocyte Biology

Pyeung-Hyeun Kim¹  Goo-Young Seo¹  Hyun-A Kim¹ 

[1] Department of Molecular Bioscience, College of Biomedical Science, Kangwon National University, Chuncheon, Republic of KoreaDepartment of Molecular Bioscience, College of Biomedical Science, Kangwon National University, Chuncheon, Republic of KoreaDepartment of Molecular Bioscience, College of Biomedical Science, Kangwon National University, Chuncheon, Republic of Korea

关键词: TGF-β;    IFN-γ;    B cell;    Ig class-switch recombination;   

DOI  :  10.1189/jlb.1209787

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

BAFF is expressed primarily by macrophages and DCs. BAFF stimulates the differentiation and survival of B cells and induces Ig production. We have demonstrated previously that murine macrophages treated with TGF-β1 or IFN-γ express membrane-bound and soluble forms of BAFF. The ability of these two forms of BAFF to induce expression of AID, which plays a critical role in Ig CSR in B cells, was investigated. Both forms of BAFF, derived from macrophages activated by IFN-γ or TGF-β1, can increase AID expression. Subsequent analysis of BAFF signaling suggested that BAFF induces AID through BCMA, a BAFF-receptor, and p38MAPK and CREB act as intermediates in AID expression. In addition, JNK and AP-1 have similar activities. Our findings suggest that macrophage-derived BAFF stimulates B cells to express AID through BCMA and at least two different pathways, including the p38MAPK/CREB and the JNK/AP-1 pathways.

【 授权许可】

Unknown