The envelope of human endogenous retrovirus in neuro-inflammation

Several lines of evidence support that its envelope protein (ENV) or its soluble extra-cellular subunit (ENV-SU) contributes to inflammation associated with the disease: 1 ENV promotes polyclonal expansion of T lymphocytes [2], 2 ENV-SU induces human monocytes and dendritic cells (DC) to produce inflammatory cytokines through engagement of CD14 and TLR4 [3]. CD14° = CD14 deficient mouse. [figure omitted; refer to PDF] Conclusion by promoting inflammatory response through CD14/TLR4 pathway, the envelope of MSRV/HERV contributes to EAE in mice and thus may be one of the key actors of MS etiology in humans.