Published ahead of print on March 23, 2004, doi:10.1165/rcmb.2003-0285OC Am. J. Respir. Cell Mol. Biol., Volume 31, Number 2, August 2004, 220-226 A more recent version of this article appeared on August 1, 2004
Submitted on July 30, 2003 Interleukin-22 (IL-22): a potential immunomodulatory molecule in the lungHayley A Whittington1,1 Division of Medicine, University of Bristol, Bristol, United Kingdom * To whom correspondence should be addressed. E-mail: ann.millar{at}bris.ac.uk.
IL-22 is a member of the human type I IFN family, which includes IL-10. IL-22 has the potential to interact with IL-10 since it binds to the IL-10R2c chain with IL-22R1 in its receptor complex. Binding can be blocked by the soluble receptor, IL-22BP. We hypothesize that IL-22 and IL-22BP are involved in inflammatory regulation and its subsequent role in the pathogenesis of inflammatory lung disease (ILD). We have demonstrated IL-22 mRNA expression in alveolar macrophages (AM), monocytes and alveolar epithelial (AE) cells. IL-22BP mRNA is expressed in AM, AE cells and neutrophils. In contrast, IL-22R1 is expressed in AE only. Immunohistochemistry on normal and ILD lung sections has confirmed IL-22 protein expression. Western blotting for IL-22 in bronchoalveolar lavage fluid demonstrated that lower levels of IL-22 were present in ARDS and sarcoidosis patients relative to controls (p=0.0152 and p=0.0213). Levels of IL-22 in IPF were not different to the controls (p=0.5838). IL-22 did not affect IL-10 inhibition of TNF-
This article has been cited by other articles:
|
|||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
in monocytes, which do not express IL-22R1. By contrast, we demonstrated synergy between IL-10 and IL-22 in terms of IL-8 inhibition in IL-22R1-expressing A549 cells. These data suggest a role for IL-22 in the regulation of pulmonary inflammation.
