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Department of Neurobiology, Swiss Federal Institute of Technology, CH-8093 Zurich, Switzerland; and
Zentrum für Molekulare Neurobiologie, Universität Hamburg, D-20246 Hamburg, Germany
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.
Key Words: lymph node L1 cell adhesion molecule fibroblastic reticular system architecture
This project was funded by National Institutes of Health grant R29 AI34562.
Abbreviations used: ANOVA, analysis of variance; CLSM, confocal laser scanning microscopy; DTH, delayed type contact hypersensitivity; FRS, fibroblastic reticular system; M
, macrophage; NRIg, normal rat immunoglobulin; RF, reticular fibroblast; RT, room temperature; TEM, transmission electron microscopy.
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