Proinflammatory CD20+ T cells contribute to CNS-directed autoimmunity
Jasmin Ochs1, Nitzan Nissimov1, Sebastian Torke1
1Institute of Neuropathology, University Medical Center, 37075 Göttingen, Germany.
CD20+ T cells acquire CD20 from B cells and are pathogenic in autoimmune diseases like MS. Eliminating these CD20+ T cells effectively treats experimental autoimmune encephalomyelitis (EAE), suggesting a therapeutic target.
Area of Science:
- Immunology
- Cell Biology
Background:
- The origin and function of CD20+ T cells remain largely unknown.
- CD20 is a B cell lineage marker, and its presence on T cells is not fully understood.
Purpose of the Study:
- To characterize CD20+ T cells in mice and humans.
- To investigate the role of CD20+ T cells in autoimmune diseases and their response to anti-CD20 antibody treatment.
Main Methods:
- Characterization of CD20+ T cells in murine and human samples.
- Investigation of CD20 acquisition via trogocytosis.
- Analysis of CD20+ T cell phenotype and function in experimental autoimmune encephalomyelitis (EAE) models.
- Assessment of therapeutic efficacy of CD20+ T cell depletion.
Main Results:
- Murine CD20+ T cells do not express CD20 endogenously; their development requires CD20+ B cells.
- T cells acquire CD20 from B cells through trogocytosis during antigen presentation.
- CD20+ T cells exhibit increased activation markers and pro-inflammatory cytokines, correlating with disease severity in EAE.
- Depletion of CD20+ T cells ameliorates EAE independently of B cells.
Conclusions:
- CD20+ T cells arise from B cell-T cell interactions and possess pathogenic potential in autoimmune disorders.
- Targeting CD20+ T cells offers a potential therapeutic strategy for multiple sclerosis (MS) and other inflammatory conditions.
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