Preservation of the delayed-type hypersensitivity response to alloantigen by xyloglucans or oligogalacturonide does not correlate with the capacity to reject ultraviolet-induced skin tumors in mice.
Preservation of the delayed-type hypersensitivity response to alloantigen by xyloglucans or oligogalacturonide does not correlate with the capacity to reject ultraviolet-induced skin tumors in mice.
复制标题
木葡聚糖或低聚半乳糖醛酸对同种抗原的迟发型超敏反应的保留与小鼠排斥紫外线诱导的皮肤肿瘤的能力无关。
DOI:
10.1046/j.1523-1747.2001.00160.x
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发表时间:
2001
期刊:
影响因子:
--
通讯作者:
Albersheim,P
中科院分区:
文献类型:
--
作者:
Strickland,FM;Sun,Y;Darvill,A;Eberhard,S;Pauly,M;Albersheim,P
Chronic exposure to ultraviolet radiation suppresses T cell-mediated immune responses and induces the formation of suppressor T lymphocytes that prevent the rejection of highly antigenic ultraviolet-induced skin cancers in mice. Tamarind seed xyloglucans and pectinic oligogalacturonides prevent suppression of delayed-type hypersensitivity immune responses in mice toCandida albicansand alloantigen caused by a single exposure of ultraviolet radiation. We therefore investigated the ability of these poly/oligosaccharides to prevent suppression of T cell-mediated immune responses and suppressor cell induction during chronic ultraviolet irradiation and to preserve the capacity of ultraviolet-irradiated mice to reject a transplanted, highly antigenic, ultraviolet-induced tumor. C3H/HeN mice were treated 3× per week for 12 wk with 15 kJ per m2ultraviolet B radiation followed by application of the polysaccharides/ oligosaccharides. The delayed-type hypersensitivity responses toC. albicansand alloantigen were measured after 1, 6, and 12 wk of treatment. Following the 12th wk of treatment the remaining mice were injected with the highly antigenic ultraviolet-induced, syngeneic tumor cell line UV5497-5. The polysaccharides/oligosaccharides protected delayed-type hypersensitivity responses toC. albicansbut not contact hypersensitivity responses to dinitrofluorobenzene for up to 6 wk of ultraviolet radiation after which protection declined and suppressor cells were observed. In contrast, the delayed-type hypersensitivity response to alloantigen was preserved for the entire 12 wk of ultraviolet irradiation. Despite protection of immunity to alloantigen, the transplanted tumor cells grew equally well in all ultraviolet-irradiated animals. These results indicate that delayed-type hypersensitivity responses are heterogeneous and that delayed-type hypersensitivity to alloantigen is not a surrogate marker for rejection of ultraviolet-induced skin tumors.