1: Allergy. 2004 May;59(5):505-14. 

Differential expression of IL-10 receptor by epithelial cells and alveolar
macrophages.

Lim S, Caramori G, Tomita K, Jazrawi E, Oates T, Chung KF, Barnes PJ, Adcock IM.

Department of Thoracic Medicine, Imperial College School of Medicine, National
Heart and Lung Institute, Dovehouse Street, London, UK.

BACKGROUND: Interleukin (IL)-10 is a pleiotropic cytokine with a broad spectrum
of immunosuppressive and anti-inflammatory effects. IL-10 secretion from
alveolar macrophages is defective in patients with asthma and lower
concentrations of IL-10 are found in bronchoalveolar lavage (BAL) from asthmatic
patients than in normal control subjects. Reduced IL-10 may result in
exaggerated and more prolonged inflammatory responses in asthmatic airways.
IL-10 acting through the IL-10 receptor (IL-10R) stimulates the transcription
factors STAT1 and STAT3. METHODS: We investigated IL-10 and IL-10R expression in
normal and asthmatic bronchial epithelium and BAL macrophages using reverse
transcription-polymerase chain reaction, immunohistochemistry and Western
blotting. The functional effect of IL-10 was examined using
granulocyte-macrophage-colony stimulating factor, enzyme-linked immunosorbent
assay and Western blotting for phosphorylated STAT1 and STAT3. RESULTS: IL-10
was not expressed in epithelial cells; furthermore these cells did not express
the IL-10R and had no functional response to exogenous IL-10. Bronchial
epithelial cells expressed variable levels of phosphorylated STAT1 and STAT3
with no change in expression between normal subjects and asthmatics. IL-10
protein and IL-10R expression was detected in alveolar macrophages from all
subjects. CONCLUSION: Our study suggests that the bronchial epithelium is not a
source of IL-10 and cannot respond to exogenous IL-10 because of a lack of
IL-10R expression.

PMID: 15080831 [PubMed - indexed for MEDLINE]


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2: Biochem J. 2003 Mar 1;370(Pt 2):391-6. 

Cloning of a new type II cytokine receptor activating signal transducer and
activator of transcription (STAT)1, STAT2 and STAT3.

Dumoutier L, Lejeune D, Hor S, Fickenscher H, Renauld JC.

The Ludwig Institute for Cancer Research, Brussels Branch, and the Experimental
Medicine Unit, Christian de Duve Institute of Cellular Pathology, Universite
Catholique de Louvain, avenue Hippocrate 74, B-1200-Brussels, Belgium.

In the present paper, we report the identification of a new gene encoding a
transmembrane protein of 520 amino acids, showing 22% amino acid identity with
the extracellular domain of the interleukin (IL)-20 receptor. This gene, termed
likely interleukin or cytokine receptor-2 ( LICR2 ), is located on chromosome 1,
at 25 kb from the IL22R (IL-22 receptor) gene, and is constitutively expressed
in most tissues. A chimaeric receptor, consisting of the extracellular domain of
the IL-10 receptor alpha chain and the intracellular domain of LICR2, activated
signal transducer and activator of transcription (STAT)1, STAT2, STAT3 and STAT5
upon IL-10 stimulation, in a Janus kinase 1-dependent manner. In contrast, none
of the IL-10-related cytokines described so far could activate LICR2-transfected
cells, suggesting that LICR2 is a signalling receptor for a new cytokine of the
IL-10 family.

PMID: 12521379 [PubMed - indexed for MEDLINE]


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