Dual role of B cells with accelerated onset but reduced disease activity in P0₁₀₆₋₁₂₅-induced experimental autoimmune neuritis of IgH ⁰(/)⁰ mice.

The role of B cells in autoimmune-mediated diseases of the peripheral nervous system was studied in experimental autoimmune neuritis (EAN) in B cell deficient IgH⁰(/)⁰ C57BL/6J mice having been immunized with P0₁₀₆₋₁₂₅ peptide. Compared to coisogenic IgH(+/+) mice, onset of EAN was accelerated [100% disease incidence at day 9 post immunization (p.i.) vs. day 15 p.i.]. At day 9 p.i., numbers of P0₁₀₆₋₁₂₅-specific interferon (IFN)-γ-producing CD4(+) T cells were increased, while IL-10 mRNA and production were decreased in IgH⁰(/)⁰ mice. Beyond day 9 p.i., declining disease activity and a significant reduction of maximal disease activity were correlated with significantly reduced numbers of IFN-γ-producing CD4(+) T cells in IgH(0/0) mice as compared with IgH(+/+) mice. Correspondingly, neuropathology demonstrated only mild axonal damage, while demyelination and dying back axonopathy with spinal cord motor neuron apoptosis were absent. Thus, depending on the stage of EAN, B cells play a dual, i.e. suppressive and enhancing, role during induction and at height of EAN, respectively. The combined interaction of B cells as well as CD4(+) and CD8(+) T cells is required for the development of EAN.