Tumor necrosis factor-α and interleukin-10 contribute to immunoparalysis in patients with acute pancreatitis

Yu Pin Ho, Cheng Tang Chiu, I. Shyan Sheen, Shu Chin Tseng, Ping Chin Lai, Shin Yi Ho, Wei Ting Chen, Tsung Nan Lin, Chun Yen Lin*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

16 Scopus citations


Immunoparalysis, defined as downregulation of human leukocyte antigen-DR (HLA-DR) expression on monocytes, is strongly associated with septic complications of acute pancreatitis. However, the possible causes of this immunoparalysis have been largely unknown. A prospective case control study was performed in 54 patients with acute pancreatitis and 24 normal volunteers. HLA-DR expression on monocytes and serum cytokine levels were measured. In addition, monocytes from normal volunteers treated with tumor necrosis factor (TNF)-α in vitro were evaluated for HLA-DR expression and cytokine release. HLA-DR expression was significantly lower in patients with severe pancreatitis than in those with mild acute pancreatitis and healthy volunteers (42.28% ± 11.49% vs. 86.85% ± 14.56% vs. 93.92% ± 7.40%, p < 0.0001). Pearson correlation analysis showed that serum TNF-α and serum interleukin-10 levels were both correlated with HLA-DR expression. In addition, exogenous TNF-α could enhance IL-10 secretion from normal monocytes in a dose-response manner. In addition, TNF-α could downregulate the HLA-DR expression on monocytes even in the presence of anti-IL-10 antibodies. Therefore, both TNF-α and IL-10 contributed to the development of immunoparalysis in patients with acute pancreatitis.

Original languageEnglish
Pages (from-to)18-23
Number of pages6
JournalHuman Immunology
Issue number1
StatePublished - 01 2011


  • Acute pancreatitis
  • HLA-DR (human leukocyte antigen-DR)
  • Immunoparalysis
  • Interleukin-10
  • Tumor necrosis factor-α


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