Ochs, J.J.OchsNissimov, N.N.NissimovTorke, S.S.TorkeFreier, M.M.FreierGrondey, K.K.GrondeyKoch, J.J.KochKlein, M.M.KleinFeldmann, L.L.FeldmannGudd, C.C.GuddBopp, T.T.BoppHäusser-Kinzel, S.S.Häusser-KinzelWeber, MartinMartinWeber2022-12-012022-12-012022https://publica.fraunhofer.de/handle/publica/42946710.1126/scitranslmed.abi46322-s2.0-8512725663735353539The origin and function of CD20+ T cells are poorly understood. Here, we characterized CD20+ T cells in mice and humans and investigated how they are affected by anti-CD20 antibody treatment. We report that murine CD20+ T cells are unable to endogenously express the B cell lineage marker CD20; the development of CD20+ T cells in rodents requires the presence of CD20-expressing B cells. Our results demonstrated that both murine and human T cells acquire CD20 from B cells via trogocytosis while being activated by an antigen-presenting B cell. In patients with multiple sclerosis (MS) and mice with experimental autoimmune encephalomyelitis (EAE), expression of CD20 on T cells is associated with an up-regulation of activation markers, proinflammatory cytokines, and adhesion molecules, suggesting high pathogenic potential. Supporting this hypothesis, CD20+ T cells expand during active EAE in rodents; furthermore, adoptive transfer of CD20+ T cells into EAE-diseased mice worsened histological and clinical severity. Of direct therapeutic relevance, we demonstrate that the exclusive therapeutic elimination of CD20+ T cells effectively ameliorates EAE, independent of B cells. The results support the hypothesis that CD20+ T cells arise upon B cell-T cell interaction and that depletion of CD20+ T cells might contribute to the success of anti-CD20 antibody therapies in MS and other inflammatory disorders.enjournal article