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<p>When immune cells interact, they frequently exchange membrane-bound antigens. Our evolving understanding of these processes challenges the cellular specificity of lineage markers and therapeutic monoclonal antibodies. By using mouse and human B-T cell co-cultures, we report that CD19, an assumingly exclusive B cell marker, is transferred via trogocytosis when B cells activate T cells. In a B cell-driven model of experimental autoimmune encephalomyelitis, CD19<sup>+</sup> T cells expand and show enhanced features of activation, differentiation, and encephalitogenic potential ex vivo. Additionally, co-transfer of CD19 and functional IgM from B cells results in the gain of B cell function by T cells. In patients with chronic central nervous system (CNS) demyelination, CD19<sup>+</sup> T cells display a pro-inflammatory phenotype and are concomitantly depleted by inebilizumab, an approved anti-CD19 antibody, which raises important considerations for the therapeutic use of monoclonal antibodies overall. Finally, we report that myeloid cells acquire CD19 and functional IgM after phagocytosis of apoptotic B cells and thereby gain functional B cell properties. These findings highlight the commonness of membrane and antigen-transfer between cells, resulting in transmission of cellular function.</p>

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B cell CD19 is transferred between immune cells in mice and humans

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月29日

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  • Jasmin Ochs,
  • Pia Schweineberg,
  • Jacqueline Thode,
  • Alica Blenkle,
  • Leila Husseini,
  • Matthias Klein,
  • Tobias Bopp,
  • Patrick Schindler,
  • Friedemann Paul,
  • Martin S. Weber

摘要

When immune cells interact, they frequently exchange membrane-bound antigens. Our evolving understanding of these processes challenges the cellular specificity of lineage markers and therapeutic monoclonal antibodies. By using mouse and human B-T cell co-cultures, we report that CD19, an assumingly exclusive B cell marker, is transferred via trogocytosis when B cells activate T cells. In a B cell-driven model of experimental autoimmune encephalomyelitis, CD19+ T cells expand and show enhanced features of activation, differentiation, and encephalitogenic potential ex vivo. Additionally, co-transfer of CD19 and functional IgM from B cells results in the gain of B cell function by T cells. In patients with chronic central nervous system (CNS) demyelination, CD19+ T cells display a pro-inflammatory phenotype and are concomitantly depleted by inebilizumab, an approved anti-CD19 antibody, which raises important considerations for the therapeutic use of monoclonal antibodies overall. Finally, we report that myeloid cells acquire CD19 and functional IgM after phagocytosis of apoptotic B cells and thereby gain functional B cell properties. These findings highlight the commonness of membrane and antigen-transfer between cells, resulting in transmission of cellular function.