Abstract
BackgroundIL-35 is a newly anti-inflammatory cytokine that belongs to the IL-12 family. Mast cells, as one of the major effector cells in the immune response system, plays an important role in the pathogenesis of chronic spontaneous urticarial (CSU). Our study aims to explore the inhibited role of IL-35 in HMC-1.MethodsThe effects of IL-35 on cell proliferation, cytokine expression, and histamine release in a human mast cell line (HMC1) were investigated by CCK8, ELISA, or RT-PCR. The phosphorylation levels of ERK1/2, p38, and JNK1/2, in PMA plus A23187 induced HMC-1 cells was detected by Western Blot.ResultsWe found that IL-35 significantly inhibited the proliferation of HMC-1 cells stimulated by PMA and A23187. IL-35 also down-regulates the release of histamine and the mRNA expression of IL-6 and IL-17 in activated HMC-1. Furthermore, IL-35 markedly inhibited the phosphorylation levels of ERK1/2, p38, and JNK1/2, in PMA plus A23187 induced HMC-1 cells.ConclusionsThis study provides the first observations on the inhibitory and anti-inflammatory effect of IL-35 in activated HMC-1 cells. We suggest that IL35 may play an inhibited role in the pathogenesis of CSU.
Highlights
IL-35 is a newly anti-inflammatory cytokine that belongs to the IL-12 family
We suggest that IL35 may play an inhibited role in the pathogenesis of chronic spontaneous urticarial (CSU)
IL‐35 receptor IL‐12R‐β2 and gp130 are expressed in HMC‐1 cells To better establish the relevance of the IL-35 pathway in CSU, we investigated the direct expression of IL-35 receptor IL-12R-β2 and gp130 in Human mast cell line (HMC-1)
Summary
IL-35 is a newly anti-inflammatory cytokine that belongs to the IL-12 family. As one of the major effector cells in the immune response system, plays an important role in the pathogenesis of chronic spontaneous urticarial (CSU). Chronic spontaneous urticarial (CSU), a mast cell-driven disease, is defined as the spontaneous appearance of weals, angioedema or both for > 6 weeks for unknown or known causes [1]. As one of the major effector cells in the immune response system, plays an important role in the pathogenesis of CSU [2]. Several studies had indicated that activated mast cells could release histamine and other cytokines, such as IL-35 is a newly anti-inflammatory cytokine that belongs to the IL-12 family and is composed of two subunits: Epstein–Barr virus-induced gene 3 (EBI3) and IL-12p35 [5].
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