HLA-G influences nasal polyp relapse in HPV positive patients.

The underlying mechanisms of nasal polyp development have yet to be determined. Human papilloma virus (HPV) infection is considered as a possible candidate, as associated with nasal inverted papilloma1. HLA-G molecule, an antigen with membrane-bound and soluble isoforms that interact with immune cell inhibitory receptors, is up-modulated by intrleukin-10 (IL-10), an anti-inflammatory cytokine, and increases during viral infection as immune-escape mechanism2. HPV infection is known to influence IL-10 and HLA-G expression3, suggesting a possible implication in nasal polyps. We investigated the influence of high risk HPV infection, IL-10 and HLA-G in nasal polyp relapses. We enrolled ten non-allergic patients with nasal polyps and analysed the presence of high-risk HPV by PCR (Sacace), the expression of HLA-G and IL-10 receptor on nasal epithelial cells by immunofluorescence (87G, IL-10R) and of sHLA-G and IL-10 by ELISA. Our results evidenced high risk HPV infection in 50% of polyps, of which the 80% presented polyp relapse (OR:15). Only HPV positive polyps expressed mHLA-G and IL-10R on epithelial cells. The analysis of nasal epithelial cell culture supernatants showed a correlation between IL-10 and sHLA-G secretion in HPV positive samples. No expression was observed in HPV negative polyps. These data suggest an association between HPV infection, up-modulation of IL-10 and HLA-G expression in nasal epithelial cells and polyp relapses.