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J. Exp. Med.,
Volume 187, Number 12, June 15, 1998 1953-1963
By
§
From the * Department of Pathology and Laboratory Medicine, Boston University School of Medicine,
Boston, Massachusetts 02118; the L1 is an immunoglobulin superfamily adhesion molecule highly expressed on neurons and involved in cell motility, neurite outgrowth, axon fasciculation, myelination, and synaptic plasticity. L1 is also expressed by nonneural cells, but its function outside of the nervous system has
not been studied extensively. We find that administration of an L1 monoclonal antibody in
vivo disrupts the normal remodeling of lymph node reticular matrix during an immune response. Ultrastructural examination reveals that reticular fibroblasts in mice treated with L1
monoclonal antibodies fail to spread and envelop collagen fibers with their cellular processes.
The induced defect in the remodeling of the fibroblastic reticular system results in the loss of
normal nodal architecture, collapsed cortical sinusoids, and macrophage accumulation in malformed sinuses. Surprisingly, such profound architectural abnormalities have no detectable effects on the primary immune response to protein antigens.
Department of Neurobiology, Swiss Federal Institute of
Technology, CH-8093 Zurich, Switzerland; and § Zentrum für Molekulare Neurobiologie, Universität
Hamburg, D-20246 Hamburg, Germany
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