The immune system functions to protect an organism against microbial infections and may be involved in the reparative response to nerve injury. The goal of this study was to determine whether the immune system plays a role in regulating motoneuron survival after a peripheral nerve injury. After a right facial nerve axotomy, facial motoneuron (FMN) survival in C.B-17 (+/+) wild-type mice was found to be 87 +/- 3.0% of the unaxotomized left side control. In contrast, facial nerve axotomy in C.B-17 (-/-) severe combined immunodeficient (scid) mice, lacking functional T and B lymphocytes, resulted in an average FMN survival of 55 +/- 3.5% relative to the unaxotomized left side control. This represented an approximately 40% decrease in FMN survival compared with wild-type controls. The reconstitution of scid mice with wild-type splenocytes containing T and B lymphocytes restored FMN survival in these mice to the level of the wild-type controls. These results suggest that immune cells associated with acquired immunity play a role in regulating motoneuron survival after a peripheral nerve injury.

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Olfactory ensheathing cells (OECs) are a unique type of macroglia required for normal olfactory axonal regeneration throughout the lifetime of an individual. Recent evidence in the literature suggests that OECs transplanted into injured spinal cords may facilitate axonal regeneration. In this study, we evaluated the neurotrophic properties of OECs using a homogeneous clonal cell line (nOEC), which does not contain contaminating cell types found in all primary OEC cultures. The results indicate that nOECs express mRNA for NGF, BDNF, NT‐4/5, and neuregulins, but not for NT‐3 or CNTF. In addition, nOECs secrete NGF, BDNF, and neuregulin, but retain NT‐4/5 intracellularly. Finally, prelabeled nOECs derived from rat survived transplantation into a dorsal hemisected region of the hamster spinal cord and migrated only in the injured, dorsal portion of the spinal cord. This migratory pattern suggests that the nOECs are viable in vivo and respond to signals originating from the injured neuronal cells and their processes. GLIA 33:225–229, 2001. © 2001 Wiley‐Liss, Inc.