Ilse, VictoriaVictoriaIlseScholz, RebekkaRebekkaScholzWermann, MichaelMichaelWermannNaumann, MarcelMarcelNaumannStaege, Martin S.Martin S.StaegeRoßner, SteffenSteffenRoßnerCynis, HolgerHolgerCynis2023-01-262023-01-262022https://publica.fraunhofer.de/handle/publica/42000210.3390/ijms23158330The triggers for the development of multiple sclerosis (MS) have not been fully understood to date. One hypothesis proposes a viral etiology. Interestingly, viral proteins from human endogenous retroviruses (HERVs) may play a role in the pathogenesis of MS. Allelic variants of the HERV-K18 env gene represent a genetic risk factor for MS, and the envelope protein is considered to be an Epstein–Barr virus-trans-activated superantigen. To further specify a possible role for HERV-K18 in MS, the present study examined the immunogenicity of the purified surface unit (SU). HERV-K18(SU) induced envelope-specific plasma IgG in immunized mice and triggered proliferation of T cells isolated from these mice. It did not trigger phenotypic changes in a mouse model of experimental autoimmune encephalomyelitis. Further studies are needed to investigate the underlying mechanisms of HERV-K18 interaction with immune system regulators in more detail.enHuman endogenous retrovirusRetroviral envelopeHERV-K18Multiple sclerosisExperimental autoimmune encephalomyelitisImmunogenicity of the envelope surface unit of human endogenous retrovirus K18 in micejournal article