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Published ahead of print on August 15, 2002, doi:10.1164/rccm.200203-217OC

Am. J. Respir. Crit. Care Med., Volume 166, Number 11, December 2002, 1475-1482

A more recent version of this article appeared on December 1, 2002
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Submitted on March 18, 2002
Accepted on July 30, 2002

Role of IL-10 in the intracellular sequestration of HLA-DR in monocytes during septic shock

Thierry Fumeaux1 and Jerome Pugin1*

1 Internal Medicine Department, Division of Medical Intensive Care, Geneva, Switzerland

* To whom correspondence should be addressed. E-mail: pugin{at}cmu.unige.ch.

Monocytes from many critically ill patients show a low expression of Major Histocompatibility Complex type II (MHC II) expression. This phenomenon is believed to play a role in these patients' increased susceptibility to secondary infections. Herein, we show that the level of monocyte HLA-DR expression inversely correlates with the degree of severity of the sepsis syndrome. The defect of the monocyte HLA-DR expression resides in an intracellular sequestration of the MHC II molecules, a post-translational effect. No significant decrease in the rate of transcription of HLA-DR, or its major transcriptional inducer, class II transactivator, was noted. The levels of HLA-DR protein produced by monocytes from patients with septic shock were comparable to those from healthy volunteers. Plasma from patients with septic shock induced significant HLA-DR endocytosis resulting in decreased surface HLA-DR expression of normal donor monocytes. This effect was partially blocked by anti-interleukin-10 (IL-10) monoclonal antibody, but not by antagonists to Transforming Growth Factor-ß1, prostaglandins or ß-adrenergic agonists. Altogether, these data suggest that HLA-DR molecules are re-endocytosed and retained intracellularly in monocytes from patients with septic shock, and that this phenomenon is partially mediated by IL-10. IL-10 may represent a future target for immunomodulating patients with the sepsis syndrome or critically ill patients at risk to develop infections.
Key words: HLA-D antigens - CIITA protein - immune paralysis - MHC II genes - antigen presentation




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