|
|||||||||
|
|
|
|
|
|
|
|
|
|
|
T Kobata, H Ikeda, Y Ohnishi, N Urushibara, TA Takahashi and S Sekiguchi
Hokkaido Red Cross Blood Center, Sapporo, Japan.
The alloreactive cytotoxic T lymphocytes (CTL) were generated by
coculturing peripheral blood mononuclear cells (PBMC) with allogeneic Sa
cells (an Epstein-Barr virus [EBV]-transformed B-cell line). The CTL did
not proliferate in response to UV-B-irradiated Sa cells unless exogenous
interleukin-2 (IL-2) was present, although they could kill the
UV-B-irradiated Sa cells. The results indicate that UV-B-irradiated Sa
cells do not provide sufficient signals for the proliferation of the CTL
while they can be recognized by CTL and induce high-affinity IL-2 receptor
(IL-2R) expression on them. The alloreactive CTL could be rendered anergic
by previous exposure to UV-B-irradiated Sa cells. The alloreactive CTL
previously stimulated with UV-B-irradiated Sa cells failed to proliferate
in response to nontreated Sa cells. Proliferation of the anergic CTL could
not be restored by Sa cells and exogenous IL-2 but by the combination of
phorbol 12-myristate 13-acetate (PMA) and calcium ionophore (A23187). The
anergic CTL showed a considerably low cytotoxic activity against Sa target
cells. The expression of TCR on the anergic CTL was downregulated while
expression of high-affinity IL- 2R was upregulated. Their CD28 and CD8
expression were unchanged. In addition, the proliferative response and
cytotoxicity of the anergic CTL to Sa cells could be restored after the
cells had been rested for 7 days to allow reexpression of TCR. These
results suggest that downregulation of T-cell receptor (TCR) and impairment
in the post-IL- 2/IL-2R signaling pathway are relevant to the clonal anergy
induced in the alloreactive CTL by stimulation of UV-B-irradiated Sa cells.
This article has been cited by other articles:
| |||||||||||
 |
 |
 |
|||||||
 |
 |
 |
 |
 |
 |
 |
 |
||
| Copyright © 1993 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
