Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2008-9-23
pubmed:abstractText
The thymus is the site where all T-cell precursors develop, mature, and subsequently leave as mature T-cells. Since the mechanisms that mediate and regulate thymic apoptosis are not fully understood, we utilized a syngenic GL261 murine glioma model to further elucidate the fate of T-cells in tumor bearing C57BL/6 mice. First, we found a dramatic reduction in the size of the thymus accompanied by a decrease in thymic cellularity in response to glioma growth in the brains of affected mice. There was a marked reduction of double positive subset and an increase in the frequency of CD4(+) and CD8(+) single positive T-cell subsets. Analysis of double negative thymocytes showed an increase in the accumulation of CD44(+) cells. In contrast, there was a marked loss of CD44 and CD122 expression in CD4(+) and CD8(+) subsets. The growth of intracranial tumors was also associated with decreased levels of HO-1, a mediator of anti-apoptotic function, and increased levels of Notch-1 and its ligand, Jagged-1. To determine whether thymic atrophy could be due to the effect of Notch and its ligand expression by glioma in vivo, we performed a bone marrow transplant experiment. Our results suggest that Notch-1 and its ligand Jagged-1 can induce apoptosis of thymocytes, thereby influencing thymic development, immune system homeostasis, and function of the immune cells in a model of experimental glioma.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0340-7004
pubmed:author
pubmed:issnType
Print
pubmed:volume
57
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1807-16
pubmed:meshHeading
pubmed-meshheading:18392618-Animals, pubmed-meshheading:18392618-Apoptosis, pubmed-meshheading:18392618-Brain Neoplasms, pubmed-meshheading:18392618-Calcium-Binding Proteins, pubmed-meshheading:18392618-Cell Differentiation, pubmed-meshheading:18392618-Disease Progression, pubmed-meshheading:18392618-Flow Cytometry, pubmed-meshheading:18392618-Glioma, pubmed-meshheading:18392618-Heme Oxygenase-1, pubmed-meshheading:18392618-Homeostasis, pubmed-meshheading:18392618-Intercellular Signaling Peptides and Proteins, pubmed-meshheading:18392618-Male, pubmed-meshheading:18392618-Membrane Proteins, pubmed-meshheading:18392618-Mice, pubmed-meshheading:18392618-Mice, Inbred C57BL, pubmed-meshheading:18392618-Receptor, Notch1, pubmed-meshheading:18392618-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:18392618-T-Lymphocyte Subsets, pubmed-meshheading:18392618-T-Lymphocytes, pubmed-meshheading:18392618-Thymus Gland
pubmed:year
2008
pubmed:articleTitle
Progression of intracranial glioma disrupts thymic homeostasis and induces T-cell apoptosis in vivo.
pubmed:affiliation
The Brain Tumor Center, The University of Chicago, 5841 S. Maryland Ave MC 3026, Chicago, IL, 60637, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't