RESUMO
Introduction: To evaluate the impact various levels of irradiation have on bone-patellar tendon-bone (BTB) allograft load-to-failure. Materials and methods: Pubmed, Google Scholar and Embase were searched for studies reporting load-to-failure measurements of BTB allografts following gamma or eBeam irradiation. All systematic reviews, editorials, as well as studies that utilized animal models and/or other graft sources (achilles, hamstring, quadriceps) were excluded. Meta-analysis was performed to compare the impact of low dose (19 ≤ kGy), intermediate (20-49 kGy) and high dose (>50 kGy) gamma and eBeam radiation on load-to-failure. Results: Twelve studies, containing a total of 429 BTB allografts (159 controls, 270 irradiated), were identified. Load-to-failure of BTB allograft was significantly decreased at intermediate (20-49 kGy) doses of radiation, while low (≤19 kGy) and high (>50 kGy) doses did not significantly change load-to-failure. Conclusions: Intermediate doses of radiation may negatively impact the biomechanical integrity of BTB allograft in vitro. Future studies are required to examine clinical outcomes at varying irradiation levels.
RESUMO
Follicular helper T (Tfh) cells are essential for germinal center (GC) B cell responses. However, it is not clear which PD-1+CXCR5+Bcl6+CD4+ T cells will differentiate into PD-1hiCXCR5hiBcl6hi GC-Tfh cells and how GC-Tfh cell differentiation is regulated. Here, we report that the sustained Tigit expression in PD-1+CXCR5+CD4+ T cells marks the precursor Tfh (pre-Tfh) to GC-Tfh transition, whereas Tigit-PD-1+CXCR5+CD4+ T cells upregulate IL-7Rα to become CXCR5+CD4+ T memory cells with or without CCR7. We demonstrate that pre-Tfh cells undergo substantial further differentiation at the transcriptome and chromatin accessibility levels to become GC-Tfh cells. The transcription factor c-Maf appears critical in governing the pre-Tfh to GC-Tfh transition, and we identify Plekho1 as a stage-specific downstream factor regulating the GC-Tfh competitive fitness. In summary, our work identifies an important marker and regulatory mechanism of PD-1+CXCR5+CD4+ T cells during their developmental choice between memory T cell fate and GC-Tfh cell differentiation.
