Mir-17–92 regulates bone marrow homing of plasma cells and production of immunoglobulin G2c

Shengli Xu (), Xijun Ou, Jianxin Huo, Kristen Lim, Yuhan Huang, Sheena Chee and Kong-Peng Lam ()
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Shengli Xu: Bioprocessing Technology Institute, Agency for Science, Technology and Research (A-STAR)
Xijun Ou: Bioprocessing Technology Institute, Agency for Science, Technology and Research (A-STAR)
Jianxin Huo: Bioprocessing Technology Institute, Agency for Science, Technology and Research (A-STAR)
Kristen Lim: Bioprocessing Technology Institute, Agency for Science, Technology and Research (A-STAR)
Yuhan Huang: Bioprocessing Technology Institute, Agency for Science, Technology and Research (A-STAR)
Sheena Chee: Bioprocessing Technology Institute, Agency for Science, Technology and Research (A-STAR)
Kong-Peng Lam: Bioprocessing Technology Institute, Agency for Science, Technology and Research (A-STAR)

Nature Communications, 2015, vol. 6, issue 1, 1-14

Abstract: Abstract The polycistronic mir-17–92 cluster, also known as oncomir-1, was previously shown to be essential for early B lymphopoiesis. However, its role in late-stage B-cell differentiation and function remains unexplored. Here we ablate mir-17–92 in mature B cells and demonstrate that mir-17–92 is dispensable for conventional B-cell development in the periphery. Interestingly, mir-17–92-deficiency in B cells leads to enhanced homing of plasma cells to the bone marrow during T-cell-dependent immune response and selectively impairs IgG2c production. Mechanistically, mir-17–92 directly represses the expression of Sphingosine 1-phosphate receptor 1 and transcription factor IKAROS, which are, respectively, important for plasma cell homing and IgG2c production. We further show that deletion of mir-17–92 could reduce IgG2c anti-DNA autoantibody production and hence mitigate immune complex glomerulonephritis in Shp1-deficient mice prone to autoimmunity. Our results identify important roles for mir-17–92 in the regulation of peripheral B-cell function.

Date: 2015
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DOI: 10.1038/ncomms7764

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