Figure 7

Merkel cell polyomavirus is one candidate IL-1 trigger in LCH. Merkel cell polyomavirus (MCPyV) may be detected by Toll-like receptors (TLRs). MyD88 is a TLR adaptor protein that binds to pERK, maintaining ERK in an active, phosphorylated state for a longer period. Activated ERK phosphorylates numerous substrates related to the expression of soluble mediators such as IL-1β. Because of the low viral load of MCPyV-DNA in LCH tissue, MCPyV does not seem to play an oncogenic role in LCH pathogenesis. MCPyV is regarded as a potential trigger of IL-1β production. Although MyD88 usually allows the activation of NF-κB, MCPyV might interfere with NF-κB activation by targeting NF-κB essential modulator (NEMO). IL-1β is synthesized as an inactive pro-form (IL-1β precursor) that accumulates in the cytosol. Cleavage of IL-1β precursor into active form requires the activation of inflammasomes.