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骨髓淋巴细胞生成的改变以及白细胞介素-6依赖的胸腺细胞分化抑制，在克氏锥虫感染期间导致胸腺萎缩。

Altered bone marrow lymphopoiesis and interleukin-6-dependent inhibition of thymocyte differentiation contribute to thymic atrophy during Trypanosoma cruzi infection.

作者信息

Carbajosa Sofía, Gea Susana, Chillón-Marinas Carlos, Poveda Cristina, Del Carmen Maza María, Fresno Manuel, Gironès Núria

机构信息

Centro de Biología Molecular Severo Ochoa, Consejo Superior de Investigaciones Científicas, Universidad Autónoma de Madrid, Cantoblanco, Madrid, Spain.

Instituto Sanitario de Investigación Princesa, Madrid, Spain.

出版信息

Oncotarget. 2017 Mar 14;8(11):17551-17561. doi: 10.18632/oncotarget.14886.

DOI:10.18632/oncotarget.14886
PMID:28147332
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5392268/
Abstract

Thymic atrophy occurs during infection being associated with apoptosis of double positive (DP) and premature exit of DP and double negative (DN) thymocytes. We observed for the first time that a significant bone marrow aplasia and a decrease in common lymphoid progenitors (CLPs) preceded thymic alterations in mice infected with Trypanosoma cruzi. In addition, depletion of the DN2 stage was previous to the DN1, indicating an alteration in the differentiation from DN1 to DN2 thymocytes. Interestingly, infected mice deficient in IL-6 expression showed higher numbers of DP and CD4+ thymocytes than wild type infected mice, while presenting similar percentages of DN1 thymocytes. Moreover, the drop in late differentiation stages of DN thymocytes was partially abrogated in comparison with wild type littermates. Thus, our results suggest that thymic atrophy involves a drop in CLPs production in bone marrow and IL-6-dependent and independent mechanisms that inhibits the differentiation of DN thymocytes.

摘要

胸腺萎缩在感染期间发生，与双阳性（DP）细胞凋亡以及DP和双阴性（DN）胸腺细胞过早离开胸腺有关。我们首次观察到，在感染克氏锥虫的小鼠中，显著的骨髓发育不全和普通淋巴祖细胞（CLP）数量减少先于胸腺改变。此外，DN2阶段的耗竭先于DN1阶段，表明从DN1到DN2胸腺细胞的分化发生了改变。有趣的是，缺乏IL-6表达的感染小鼠比野生型感染小鼠表现出更多的DP和CD4 +胸腺细胞，而DN1胸腺细胞的百分比相似。此外，与野生型同窝小鼠相比，DN胸腺细胞晚期分化阶段的下降部分得到缓解。因此，我们的结果表明，胸腺萎缩涉及骨髓中CLP产生的下降以及抑制DN胸腺细胞分化的IL-6依赖性和非依赖性机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/538c/5392268/ede4a96d2b42/oncotarget-08-17551-g007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/538c/5392268/b8400e7e7aca/oncotarget-08-17551-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/538c/5392268/739292e0b5c4/oncotarget-08-17551-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/538c/5392268/ede4a96d2b42/oncotarget-08-17551-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/538c/5392268/8287ae3d6cba/oncotarget-08-17551-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/538c/5392268/cce2f8b3f49d/oncotarget-08-17551-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/538c/5392268/a322435bbfb2/oncotarget-08-17551-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/538c/5392268/3f44b53aedda/oncotarget-08-17551-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/538c/5392268/b8400e7e7aca/oncotarget-08-17551-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/538c/5392268/739292e0b5c4/oncotarget-08-17551-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/538c/5392268/ede4a96d2b42/oncotarget-08-17551-g007.jpg

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