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感染克氏锥虫的小鼠的接触敏感性反应。

Contact sensitivity responses in mice infected with Trypanosoma cruzi.

作者信息

Reed S G, Larson C L, Speer C A

出版信息

Infect Immun. 1978 Nov;22(2):548-54. doi: 10.1128/iai.22.2.548-554.1978.

Abstract

Mechanisms of depression of contact sensitivity responses in C57BL/10 mice infected with Trypanosoma cruzi were studied. Cellular involvement during sensitization with oxazolone was investigated in mice acutely infected with T. cruzi. Contact sensitivity was not expressed in mice during the latter stages of the acute infection. Spleen cells from sensitized, infected mice which were unable to respond to oxazolone could confer contact sensitivity upon normal syngenic mice as effectively as spleen cells from uninfected, sensitized donors. The ability of mice infected with T. cruzi to respond to an eliciting dose of oxazolone was significantly improved when macrophages from normal syngenic donors were administered to them at the time of skin test. When either normal or infected mice were used as recipients of lymphocytes from sensitized donors, the normal mice responded significantly better than did infected mice after administration of an eliciting dose of oxazolone. An increase in pyroninophilic cells was observed in draining lymph nodes after application of a sensitizing dose of oxaxolone to the ears of either normal or acutely infected mice. These results indicate that suppression of contact sensitivity during acute T. cruzi infection is directed toward the efferent arm rather than the afferent arm of the response.

摘要

研究了感染克氏锥虫的C57BL/10小鼠接触敏感性反应降低的机制。在急性感染克氏锥虫的小鼠中,研究了用恶唑酮致敏期间的细胞参与情况。在急性感染的后期,小鼠未表现出接触敏感性。来自致敏、感染但无法对恶唑酮产生反应的小鼠的脾细胞,能够像来自未感染、致敏供体的脾细胞一样有效地赋予同基因正常小鼠接触敏感性。当在皮肤试验时给感染克氏锥虫的小鼠注射来自同基因正常供体的巨噬细胞时,它们对激发剂量恶唑酮的反应能力显著提高。当正常或感染小鼠作为致敏供体淋巴细胞的受体时,在给予激发剂量的恶唑酮后,正常小鼠的反应明显优于感染小鼠。在给正常或急性感染小鼠的耳部施用致敏剂量的恶唑酮后,在引流淋巴结中观察到嗜派洛宁细胞增加。这些结果表明,急性克氏锥虫感染期间接触敏感性的抑制是针对反应的传出臂而非传入臂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/69b8/422190/72bb43c099b0/iai00203-0252-a.jpg

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