Moreover, this overexpression could contribute, for example, to an increase in the antigen-presentation rate in monocytes or to the aberrant activation of cells which barely express pHERV-W ENV proteins, such as T lymphocytes, through proinflammatory factors release (in fact, CD4+ T lymphocyte activation through TLR4 receptors leads to a boost of autoimmune processes in experimental autoimmune encephalomyelitis, the mouse model of MS (30)). This evidence concerns the gene CD4 and experimental autoimmune encephalomyelitis.