Interleukin-1beta triggers the expansion of circulating granulocytic myeloid-derived suppressor cell subset dependent on Erk1/2 activation

  • Immunobiology. 2022 Jan;227(1):152165. doi: 10.1016/j.imbio.2021.152165.
Huifang Shi  1 ,  Yan Qin  2 ,  Yufeng Tian  2 ,  Jiaan Wang  3 ,  Yan Wang  4 ,  Ziyi Wang  5 ,  Jie Lv  6
Affiliations
  • 1. Clinical Laboratory, The Rizhao People's Hospital Affiliated to Jining Medical University, Rizhao, Shandong, China. Electronic address: [email protected].
  • 2. Clinical Laboratory, The Rizhao People's Hospital Affiliated to Jining Medical University, Rizhao, Shandong, China.
  • 3. Department of Blood Transfusion, The Rizhao People's Hospital Affiliated to Jining Medical University, Rizhao, Shandong, China.
  • 4. Department of Medical Image, The Rizhao People's Hospital Affiliated to Jining Medical University, Rizhao, Shandong, China.
  • 5. Department of Anesthesiology, The Rizhao People's Hospital Affiliated to Jining Medical University, Rizhao, Shandong, China.
  • 6. Clinical Laboratory, The Rizhao People's Hospital Affiliated to Jining Medical University, Rizhao, Shandong, China. Electronic address: [email protected].
PMID: 34936966 DOI: 10.1016/j.imbio.2021.152165
Abstract

Chronic inflammation contributes to Cancer development and progression. Although interleukin-1beta (IL-1β) has been observed to be associated with an general immune suppression of T cell response and the immunosuppression strongly correlates with accumulation of myeloid-derived suppressor cells (MDSCs), the relationship and mechanism between MDSCs expansion and IL-1β expression remain ambiguous. Here, we showed that the concentration of IL-1β was highly correlated with G-MDSC subset, rather than mo-MDSC subset. Recombinant IL-1β increased the percentage of G-MDSCs in the blood of tumor-bearing mice, and IL-1RA attenuated the accumulation of G-MDSCs in the tumor-bearing mice. In addition, the IL-1β-overexpressing B16F10 cells induced higher level of G-MDSCs compared with wild-type B16F10 cells. Moreover, we found that the accumulation of G-MDSCs induced by IL-1β was dependent on the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2). Collectively, these findings show a novel role of IL-1β in G-MDSCs accumulation by activating ERK1/2, which suggests that IL-1β elimination or ERK1/2 signaling blockade could decrease G-MDSCs generation and thereby improve host immunosurveillance.

Keywords
Expansion; Extracellular regulated protein kinase 1/2; Granulocytic myeloid-derived suppressor cell; Interleukin-1beta; Interleukin-6.
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