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Pro-IL-16 Is Associated With MHC Class II-mediated Negative Regulation of Mouse Resting B Cell Activation Through MAP Kinases, NF-κB and Skp2-dependent p27kip Regulation

H-Y Yang, J Kim, S-H Kim, C-H Choe, Y-S Jang

Scand J Immunol. 2013 Mar;77(3):177-86.

PMID: 23297678

Abstract:

MHC class II molecules, in addition to their essential role as antigen-presenting molecules to CD4(+) T cell receptor, have a signal-transducing role related to B cell function. We identified pro-IL-16 as one of the proteins associated with MHC class II-mediated signalling in an analysis of MHC class II-associated molecules using immunoprecipitation and proteomics data obtained from the 38B9 resting B cell line, and investigated the role of pro-IL-16 in resting B cell activation. We found that pro-IL-16, rather than mature form of IL-16, is present both in the cytoplasm and nucleus of resting B cells, and its expression is influenced by MHC class II-mediated signalling. In addition, overexpression of pro-IL-16 impaired resting B cell proliferation and this inhibitory effect was mediated through regulating nuclear factor (NF)-κB activation. Knock-down of pro-IL-16 expression using siRNA decreased the level of cell-cycle inhibitor p27(kip) and increased the level of Skp2. In addition, knock-down of pro-IL-16 modulated mitogen-activated protein kinase activation. Given that IL-16 acts as an immunomodulator by impairing antigen-induced T cell activation and its precursor, pro-IL-16, plays a role in regulating the cell cycle in T lymphocytes and T cell lymphoma, we concluded that pro-IL-16 is involved in resting B cell proliferation, similar to its function in T lymphocytes.

Chemicals Related in the Paper:

Catalog Number Product Name Structure CAS Number Price
IAR42413356 IL-16 from mouse IL-16 from mouse Price
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