Metastatic triple negative breast cancer poses a significant health challenge due to rapid progression and limited treatment options. Immunotherapies targeting T cell responses against metastatic tumors depend on the presence of specific T cell phenotypes, which dynamically evolve with disease progression and treatment. Herein, we investigate T cell phenotype dynamics throughout metastatic disease progression, focusing on both the metastatic site in the lung and a biomaterial implant that serves as a synthetic metastatic niche, with the latter providing an accessible, non-vital tissue for longitudinal analysis. Regulatory T cells were reduced at the lung and scaffold implant sites of metastasis following disease onset and progression relative to healthy mice, while Th1 and Th17 populations remained relatively stable. CD8+ T cells transitioned from naïve and central memory to effector memory with disease progression. Additionally, functional analyses involving the metastatic tissues suggested the primary T cell suppressive mechanisms was reduced migration, with no impact on T cell activation. Blood-based analyses demonstrated some of these phenotypic dynamics yet does not recapitulate the functional assays. Collectively, the scaffold provides a platform for dynamically monitoring T cell phenotypes and functions similar to the metastatic lung, enabling longitudinal monitoring of disease progression that could stratify patient populations.
Longitudinal Monitoring of T cell Dynamics in Metastatic Breast Cancer via a Remote Diagnostic Implant.
通过远程诊断植入物对转移性乳腺癌中的T细胞动态进行纵向监测
阅读:5
作者:Schrack Ian A, Pereles Rebecca S, Ross Brian C, Ma Jeffrey A, Urie Russell R, Irish Emily R, Escalona Guillermo, Griffin Kate V, Kang Kathryn, Jeruss Jacqueline S, Shea Lonnie D
| 期刊: | Immunomedicine | 影响因子: | 0.000 |
| 时间: | 2024 | 起止号: | 2024 Dec |
| doi: | 10.1002/imed.70000 | 研究方向: | 细胞生物学 |
| 疾病类型: | 乳腺癌 | ||
特别声明
1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。
2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。
3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。
4、投稿及合作请联系:info@biocloudy.com。
