Effect of Stilbene-Type Anion Channel Blockers on the Immune Response During Experimental Allergic Neuritis (EAN)
作者:
MixEilhard,
CorrealeJ.,
OlssonT.,
SoldersG.,
LinkH.,
期刊:
Immunopharmacology and Immunotoxicology
(Taylor Available online 1992)
卷期:
Volume 14,
issue 3
页码: 579-609
ISSN:0892-3973
年代: 1992
DOI:10.3109/08923979209005412
出版商: Taylor&Francis
数据来源: Taylor
摘要:
AbstractWe have studied the role of anion channel gating for the autoimmune response in experimental allergic neuritis (EAN) induced by bovine peripheral myelin (BPM). The influence of the stilbene-type anion channel blockers SITS and DIDS on T cell function was assessed by measurement of proliferation and by counting of interferon-gamma (IFN-γ) secreting cells (IFN-γ-sc) in response to BPM and phytohemagglutinin (PHA). SITS caused a dose-dependent increase of spontaneous proliferative activity as well as of proliferation in response to the antigenic stimulus BPM. In contrast, the drug caused a decrease of proliferation of cells stimulated with PHA. The number of cells induced to IFN-γsecretion was reduced by SITS. The suppressive effect was dependent on the degree of activity of cells without drugs. Cultures showing high numbers of BPM reactive T cells were more easily suppressed than cultures with low numbers of BPM reactive T cells. Our results suggest that anion channel gating is involved in the triggering of T cells to IFN-γsecretion. The anion channel signal pathway in lymphocytes could be a target for pharmacological intervention in inflammatory disorders. In the presently used autoimmune model, EAN, the net effect of in vivo treatment with SITS resulted in worsening of clinical signs and increased inflammatory cell infiltration in sciatic nerve, whereas the in vitro conductivity of sciatic nerve was not significantly affected by the drug. Thus anion channel gating seems to regulate activities of immune cells, and drugs with anion channel blocking properties may have effects that enhance autoimmune disease.
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