S. Dijkstra et al., Up-regulation of CD81 (target of the antiproliferative antibody; TAPA) by reactive microglia and astrocytes after spinal cord injury in the rat, J COMP NEUR, 428(2), 2000, pp. 266-277
We examined the expression of CD81 (also known as TAPA, or target of the an
tiproliferative antibody) after traumatic spinal cord injury in the rat. CD
81, a member of the tetraspanin family of proteins, is thought to be involv
ed in reactive gliosis. This is based on the antiproliferative and antiadhe
sive effects of antibodies against CD81 on cultured astrocytes, as well as
its up-regulation after penetrating brain injury. CD81 expression following
dorsal hemisection of the spinal cord was determined immunohistochemically
at time points ranging from 1 day to 2 months postlesion (p.l.). In the un
lesioned cord a low background level of CD81 was observed, with the excepti
on of the ependyma of the central canal and the pia mater, which were stron
gly CD81-positive. One day p.l., CD81 was diffusely up-regulated in the spi
nal cord parenchyma surrounding the lesion site. From 3 days onward, intens
ely CD81-positive round cells entered the lesion site, completely filling i
t by 7 days p.l. Staining with the microglial markers OX-42 and Iba1 reveal
ed that these cells were reactive microglia/ macrophages. At this time, no
significant CD81 expression by GFAP-positive reactive astrocytes was noted.
From the second week onward, CD81 was gradually down-regulated; i.e., its
spatial distribution became more restricted. The CD81-positive microglia/ma
crophages disappeared from the lesion site, leaving behind large cavities.
After 2 months, astrocytes that formed the wall of these cavities were stro
ngly CD81-positive. In addition, CD81 was present on reactive astrocytes in
the dorsal funiculus distal from the lesion in degenerated white matter tr
acts. In conclusion, the spatiotemporal expression pattern of CD81 by react
ive microglia and astrocytes indicates that CD81 is involved in the glial r
esponse to spinal cord injury. (C) 2000 Wiley-Liss, Inc.