Antibodies accumulate in peripheral nerves of myelin mutant mice. (A) Immunohistochemical localization of endogenous antibodies (IgG) in the femoral quadriceps (q) and saphenous nerve (s) from 6-month-old wildtype mice (P0wt) and myelin mutants (P0het). Note the prominent labeling of the endoneurium in nerve cross sections in femoral quadriceps nerves of mutants in contrast to wildtype mice. RAG1-deficient mice (deficient for T- and B-lymphocytes) are, expectedly, devoid of antibody deposition. Scale bar, 20 µm. (B) IgG fluorescence intensity in the endoneurium of femoral quadriceps nerve cross sections is shown as the mean gray value, taking P0wt nerves as a reference. n = 2 animals per genotype were analyzed within three repeated stainings and measurements. (C) Immunohistochemical localization of endogenous antibodies (IgG) in the femoral quadriceps (q) and saphenous nerve (s) from 1-month-old wildtype mice (P0wt) and myelin mutants (P0het). Note similar endoneurial immunoreactivity in comparison to 6-month-old mutants (see A), but the lower intensity of the perineurium. Scale bar, 20 µm. (D) Immunocytochemical staining against IgG on single fiber preparations. Note preferential deposition of antibodies in the nodal regions and the generally stronger signal along myelinated fibers in P0het mice compared to wildtype mice. Nerve-specific antibodies are not detectable in RAG1-deficient mice. The corresponding phase contrast micrograph displays the teased fiber with