L1 ANTIBODIES BLOCK LYMPH-NODE FIBROBLASTIC RETICULAR MATRIX REMODELING IN-VIVO

L1 is an immunoglobulin superfamily adhesion molecule highly expressed on neurons and involved in cell motility, neurite outgrowth, axon fas ciculation, myelination, and synaptic plasticity. L1 is also expressed by nonneural cells, but its function outside of the nervous system ha s not been studied extensively. We find that administration of an L1 m onoclonal antibody in vivo disrupts the normal remodeling of lymph nod e reticular matrix during an immune response. Ultrastructural examinat ion reveals that reticular fibroblasts m mice treated with L1 monoclon al antibodies fail to spread and envelop collagen fibers with their ce llular processes. The induced defect in the remodeling of the fibrobla stic reticular system results in the loss of normal nodal architecture , collapsed cortical sinusoids, and macrophage accumulation in malform ed sinuses. Surprisingly, such profound architectural abnormalities ha ve no detectable effects on the primary immune response to protein ant igens.