有哪些信誉好的足球投注网站acute endotoxin-induced thymic atrophy is characterized by intrathymic inflammatory and wound healing responses急性endotoxin-induced胸腺萎缩的特征是intrathymic炎症和伤口愈合反应.pdfVIP
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acute endotoxin-induced thymic atrophy is characterized by intrathymic inflammatory and wound healing responses急性endotoxin-induced胸腺萎缩的特征是intrathymic炎症和伤口愈合反应
Acute Endotoxin-Induced Thymic Atrophy Is
Characterized By Intrathymic Inflammatory and Wound
Healing Responses
1 2 2
Matthew J. Billard , Amanda L. Gruver , Gregory D. Sempowski *
1 Department of Biostatistics Bioinformatics, Duke University Medical Center, Durham, North Carolina, United States of America, 2 Department of Medicine, Department
of Pathology, and the Duke University Human Vaccine Institute, Duke University Medical Center, Durham, North Carolina, United States of America
Abstract
Background: Productive thymopoiesis is essential for a robust and healthy immune system. Thymus unfortunately is acutely
sensitive to stress resulting in involution and decreased T cell production. Thymic involution is a complication of many
clinical settings, including infection, malnutrition, starvation, and irradiation or immunosuppressive therapies. Systemic rises
in glucocorticoids and inflammatory cytokines are known to contribute to thymic atrophy. Little is known, however, about
intrathymic mechanisms that may actively contribute to thymus atrophy or initiate thymic recovery following stress events.
Methodology/Principal Findings: Phenotypic, histologic and transcriptome/pathway analysis of murine thymic tissue
during the early stages of endotoxemia-induced thymic involution was performed to identify putative mechanisms that
drive thymic involution during stress. Thymus atrophy in this murine model was confirmed by down-regulation of genes
involved in T cell development, cell activation, and cell cycle progression, correlating with observed phenotypic and
histologic thymus involution. Significant gene changes support the hypothesis that multiple key intrathymic pathways are
differentially activated during stress-i
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