B cells play an important role in host immunity. B cell activation is initiated by the antigen recognition of the B cell receptor (BCR), leading to the production of antibodies against pathogenic invaders [1]. Besides the BCR, several costimulatory receptors expressed on B cells can also regulate B cell proliferation, survival, and antibody production. These include CD19, CD40, CD1d, Toll-like receptors (TLRs), and other molecules [[2], [3], [4], [5], [6]]. In addition, microRNAs (miRNAs) have been found to be involved in the regulation of B cells in a post-transcriptional way.

MiRNAs are an abundant class of endogenous non-coding small RNAs, approximately 22 nucleotides in length, which can regulate gene expression by forming a protein complex known as the RNA-induced silencing complex (RISC) together with Argonaute (AGO) protein [7]. A single miRNA can act on multiple mRNAs, and a single mRNA can be regulated by multiple miRNAs. Thus, miRNAs constitute a complex biological regulatory network. Numerous studies have shown that miRNAs participate in B cell development, activation, survival and functions. For example, miR-26, miR-191, miR-29c and miR-125b are involved in B cell development [[8], [9], [10], [11]]. Besides, miR-29 and miR-582 regulates B cell survival [12,13]. With regard to B cell activation, Gianfranco Ferraccioli et al. found that miR-155 might be a regulator of B cell activation in patients with rheumatoid arthritis (RA) by regulating the expression of PU.1 [14]. Moreover, miR-152-3p has been found to control B cell activation level and its production of BAFF [15].

The gene encoding miR-130b primary transcript is situated in murine chromosome 16. It has been found that miR-130b can promote tumor progression in leiomyosarcoma through miR-130b-TSC1 pathway [16]. Besides, miR-130b/301b represses beige adipogenesis via PGC-1α and AMPK signaling [17]. Moreover, miR-130b is upregulated in leukemic blasts and controls the transition from preleukemic to acute leukemia [18]. In addition, it has been reported that miR-130b participates in skeletal muscle regeneration targeting Sp1 [19]. However, the role of miR-130b in the process of B cell activation remains unclear.

CYLD is a deubiquitination enzyme to be involved in cancer, inflammation and cell death [20]. It has been found to negatively regulate NF-κB signaling through targeting TRAF2, TRAF6, TAK1 and NEMO [[21], [22], [23], [24]]. Also, CYLD regulates intestinal inflammation by the way of deubiquitinating NLRP6 inflammasome [25]. Besides, CYLD regulates apoptosis and necrosis via RIPK1 [26,27]. Moreover, CYLD also regulates B cell homeostasis and activation in both positive and negative ways according to its splice variants [28].

In this study, we first found that miR-130b was differentially expressed in B cells at different developmental stages from Pro/Pre-B cells to mature B cells and its expression decreased after B cell activation. Furthermore, it has been suggested that miR-130b overexpression promoted the proliferation of B cells and inhibited B cell apoptosis. At the same time, miR-130b might exert its function by targeting Cyld, thereby affecting the NF-κB signaling. In conclusion, our findings indicate that miR-130b plays a vital role in B cell proliferation and apoptosis.