COMPARISON OF THE GROWTH AND FATE OF FETAL SPINAL ISOGRAFT AND ALLOGRAFT IN THE ADULT-RAT INJURED SPINAL-CORD

Citation
Dp. Theele et al., COMPARISON OF THE GROWTH AND FATE OF FETAL SPINAL ISOGRAFT AND ALLOGRAFT IN THE ADULT-RAT INJURED SPINAL-CORD, Experimental neurology, 142(1), 1996, pp. 128-143
Citations number
70
Categorie Soggetti
Neurosciences
Journal title
ISSN journal
00144886
Volume
142
Issue
1
Year of publication
1996
Pages
128 - 143
Database
ISI
SICI code
0014-4886(1996)142:1<128:COTGAF>2.0.ZU;2-A
Abstract
Most studies investigating early fetal CNS graft-host interactions and host immune responses have been performed using intracerebral transpl antation paradigms. The purpose of this study was to establish the ear ly developmental dynamics of fetal graft integration with the injured host spinal cord and to determine whether fetal allografts in this env ironment are subject to rejection. ACI rat fetal spinal cord (FSC) tis sue was grafted into acute lesion cavities of adult WF rat spinal cord s. Graft development and/or rejection was followed from 1 to 45 days p osttransplantation with morphometric, histological, and immunocytochem ical methods, We determined that all FSC grafts in acute resection les ions of the adult rat spinal cord undergo an early substantial cellula r attrition, but following favorable attachment to healthy host tissue margins, they rebound and grow to fill the lesion cavity by approxima tely 45 days. We also determined that FSC allografts into nonimmunosup pressed adult recipients are consistently rejected, but only after an early period of growth and maturation. The onset of rejection is chara cterized by extensive cellular infiltration coincidental with graft an d host MHC antigen expression. The implications of delayed graft devel opment and graft-host integration are discussed relative to inter-conn ectivity and long-term potential for graft-derived benefits. The obser ved rejection response was characteristic of first-order allograft rej ection and underscores a lack of immunological privilege in the microe nvironment of the injured spinal cord. (C) 1996 Academic Press, Inc.