Journal
JOURNAL OF INVESTIGATIVE DERMATOLOGY
Volume 130, Issue 5, Pages 1337-1344Publisher
ELSEVIER SCIENCE INC
DOI: 10.1038/jid.2009.433
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Funding
- Institut National de la Sante et de la Recherche Medicale (INSERM)
- Universite Paul Sabatier
- Toulouse III
- Centre National de la Recherche Scientifique (CNRS)
- Universite Pierre et Marie Curie Paris VI
- la Ligue contre le Cancer comites du Tarn et Garonne et du Gers
- Fondation de la Recherche Medicale
- Association pour la Recherche sur le Cancer
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Endogenous opioid peptides mainly produced by neurons are also released by immune cells. They bind to mu- (mu-opioid receptor, MOR), delta-, and kappa-opioid receptors. On the basis of studies on mice showing that MOR is the main mediator of the deleterious effects of opioids on immunity, we wondered whether MOR, absent under normal conditions, is expressed in some pathological situations such as lymphomas. mRNA expression for all three opioid receptors was examined in lymph node biopsy samples from patients with non-Hodgkin's B-cell and T-cell lymphomas. We found that MOR and one of its ligands (enkephalin) are simultaneously expressed almost exclusively in lymph nodes from patients with Sezary cutaneous T cell lymphoma. As MOR was undetectable in circulating malignant T lymphocytes and in normal immune cells, we hypothesized that tumor-released cytokines might induce MOR expression in non-neoplastic lymph node cells. The correlation between mRNA levels of MOR and interleukin-13 (IL-13) within lymph nodes from Sezary patients led us to investigate the ability of IL-13 to upregulate MOR expression in normal immune cell subsets. We found that IL-13 upregulates MOR in activated Langerhans cells. Thus, our data suggest that, under pathological conditions, IL-13 overexpression might allow immune-derived endogenous opioids to down-modulate immune response.
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