The action of cortisone acetate on cell-mediated immunity to infection. Suppression of host cell proliferation and alteration of cellular composition of infective foci.
The action of cortisone acetate on cell-mediated immunity to infection. Suppression of host cell proliferation and alteration of cellular composition of infective foci.
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DOI：
10.1084/jem.134.6.1485
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发表时间：
1971-12-01
影响因子：
15.3
通讯作者：
NORTH, RJ
中科院分区：
文献类型：
--
作者：
NORTH, RJ
用氚标记的胸腺嘧啶核苷脉冲标记表明，小鼠对感染单核细胞增多性李斯特氏菌的反应包括脾淋巴细胞分裂大量增加，肝脏巨噬细胞分裂增加，单核细胞来源的巨噬细胞在组织中的感染灶处聚集。在感染开始时，单剂量2.5毫克的可的松就会大大延迟和抑制宿主反应的这三个组成部分。可的松治疗后细菌的无限制繁殖最终是因为单核细胞来源的巨噬细胞未能在感染灶聚集，在那里它们通常表现出免疫力。相反，这些位点的多态积累得到了增强。有人认为，醋酸可的松通过抑制脾中免疫结合淋巴细胞的产生间接防止单核细胞在感染灶聚集，而淋巴细胞是介导感染灶细胞事件所必需的。
Pulse labeling with tritiated thymidine shows that the response in the mouse to infection with L. monocytogenes includes a large increase in the division of lymphoid cells in the spleen, an increase in the division of macrophages in the liver, and an accumulation of monocyte-derived macrophages at infective foci in the tissues. A single 2.5 mg dose of cortisone acetate given at the beginning of infection greatly delays and suppresses these three components of the host response. The unrestricted bacterial multiplication which follows cortisone treatment is ultimately because of a failure of monocyte-derived macrophages to accumulate at infective foci where they normally express immunity. The accumulation of polymorphs at these sites, in contrast, is enhanced. It is argued that cortisone acetate prevents the accumulation of monocytes at infective foci indirectly by suppressing the production in the spleen of immunologically-committed lymphocytes which are needed to mediate the cellular events at infective foci.
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影响因子：
7.8
作者：
CARO, LG;KOLB, JA;VANTUBERGEN, RP
通讯作者：
VANTUBERGEN, RP
影响因子：
15.3
作者：
THOMPSON J;VAN FURTH R
通讯作者：
VAN FURTH R
DOI：
10.1084/jem.130.2.299
发表时间：
1969-08-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
North RJ
通讯作者：
North RJ
影响因子：
3.2
作者：
ALLISON, F;ADCOCK, MH
通讯作者：
ADCOCK, MH
化学抑制适应性免疫。
影响因子：
--
作者：
Gabrielsen, A E;Good, R A
通讯作者：
Good, R A