The neonatal injection of semi-allogeneic spleen cells in mice induces a state of tolerance which can be demonstrated in mixed lymphocyte culture by the inability of T lymphocytes to proliferate, to secrete interleukin-2 and to generate cytolytic activities towards the injected alloantigens. Tolerant animals develop an autoimmune syndrome characterized by an antibody-mediated glomerulonephritis associated with high levels of IgE, IgG1 and anti-DNA antibodies. This syndrome is linked to the activation of B cells injected at birth by host T cells which escape tolerance induction. Interleukin 4 is one of the mediators of these lymphocytic interactions, which suggests that Th2 cells play an important role in this experimental model of autoimmune glomerulonephritis.
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