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

Acta Neuropathologica
Anna BrunnMartina Deckert

Abstract

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.

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Citations

Mar 13, 2014·ILAR Journal·Betty Soliven
Sep 12, 2012·Journal of Neuropathology and Experimental Neurology·Anna BrunnMartina Deckert
Apr 9, 2014·Journal of Neuropathology and Experimental Neurology·Anna BrunnMartina Deckert
Oct 15, 2013·Clinical and Experimental Immunology·P M AbrahamB Soliven

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