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International Immunology, Vol. 12, No. 11, 1483-1497, November 2000
© 2000 Japanese Society for Immunology

Self-limiting systemic autoimmune disease during reconstitution of T cell-deficient mice with syngeneic T cells: support for a multifaceted role of T cells in the maintenance of peripheral B cell tolerance

Vicky M. Lentz and Tim Manser

Department of Microbiology and Immunology, and the Kimmel Cancer Institute, BLSB 708 ,233 South 10th Street, Jefferson Medical College, Philadelphia, PA 19107, USA

Correspondence to: T. Manser

The T cell compartment can be partially reconstituted in mice with targeted inactivation of the TCR Cß and C{delta} genes by injection of mature, syngeneic T cells. Surprisingly, during this reconstitution high titers of IgG anti-nuclear antibodies and symptoms of systemic autoimmune disease develop. However, this autoimmune response is transient and aged, reconstituted mice show no overt signs of disease. The autoantibody response appears to be derived from a pre-existing population of host self-reactive B cells and requires CD40 ligand-mediated co-stimulation from donor cells. Diminution of this response is coincident with a vigorous germinal center reaction and the disappearance of a subpopulation of activated B cells that expresses elevated levels of Fas. Collectively, our data support the idea that T cells play a multifaceted role in the maintenance of peripheral B cell tolerance that includes mediating the activation-induced death of autospecific B cells.

Keywords: antigens, autoantibodies, CD95, clonal deletion, germinal centers, immunohistochemistry

Transmitting editor: R. Hardy


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