Details

Autor(en) / Beteiligte

• Vermi, William
• Fisogni, Simona
• Salogni, Laura
• Schärer, Leo
• Kutzner, Heinz
• Sozzani, Silvano
• Lonardi, Silvia
• Rossini, Cristina
• Calzavara-Pinton, Piergiacomo
• LeBoit, Philip E.
• Facchetti, Fabio

Titel

Spontaneous Regression of Highly Immunogenic Molluscum contagiosum Virus (MCV)-Induced Skin Lesions Is Associated with Plasmacytoid Dendritic Cells and IFN-DC Infiltration

Ist Teil von

• Journal of investigative dermatology, 2011-02, Vol.131 (2), p.426-434

Ort / Verlag

New York, NY: Elsevier Inc

Erscheinungsjahr

2011

Quelle

MEDLINE

Beschreibungen/Notizen

• Molluscum contagiosum virus (MCV) infection induces self-limiting cutaneous lesions in an immunocompetent host that can undergo spontaneous regression preceded by local inflammation. On histology, a large majority of MCV-induced lesions are characterized by islands of hyperplastic epithelium containing infected keratinocytes and surrounded by scarce inflammatory infiltrate. However, spontaneous regression has been associated with the occurrence of a dense inflammatory reaction. By histology and immunohistochemistry, we identified MCV-induced lesions showing a dense inflammatory infiltrate associated with cell death in keratinocytes (inflammatory Molluscum contagiosum (I-MC)). In I-MC, hyperplastic keratinocytes were highly immunogenic as demonstrated by the expression of major histocompatibility complex class I and II molecules. Immune cell infiltration consisted of numerous cytotoxic T cells admixed with natural killer cells and plasmacytoid dendritic cells (PDCs). Accordingly, a type I IFN signature associated with PDC infiltration was demonstrated in both keratinocytes and inflammatory cells. Among the latter, a cell population resembling IFN-DC (CD123+CD11c+CD16+CD14+MxA+) was identified in proximity to islands of apoptotic keratinocytes. In vitro–generated IFN-DCs expressed a strong cytotoxic signature, as demonstrated by high levels of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and Fas ligand (FasL). This study establishes a previously unreported model to underpin the role of innate immune cells in viral immune surveillance.