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Status |
Public on Sep 22, 2009 |
Title |
Transcriptional profiling of p56lck-deficient regulatory and memory T cells |
Organism |
Mus musculus |
Experiment type |
Expression profiling by array
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Summary |
Signaling through the T cell antigen receptor is essential for the formation of regulatory T (Treg) cells in the thymus and for their involvement in antigen-directed suppression of immune responses. Using a conditional null allele of the gene encoding p56Lck we show here that T cell antigen receptor (TCR) signaling is also essential for sustaining the phenotype and homeostasis of Treg cells. Inactivation of p56Lck in Treg cells resulted in large-scale changes in their gene expression profile, blocked their capacity to suppress responses, inhibited their proliferation, and caused them to redistribute in the body. The results make clear multiple aspects of the Treg cell phenotype that are dependent on a sustained capacity to respond through their TCRs.
Keywords: Genetic deficiency of p56lck
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Overall design |
Two-condition experiment: wild-type memory or regulatory T cells versus lck-deficient memory or regulatory T cells.
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Contributor(s) |
Killeen N, Klinger M |
Citation(s) |
19668367 |
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Submission date |
Nov 18, 2008 |
Last update date |
Feb 17, 2015 |
Contact name |
Mark Klinger |
E-mail(s) |
mark.klinger@ucsf.edu
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Phone |
415-502-5432
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Organization name |
University of California, San Francisco
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Department |
Microbiology and Immunology
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Lab |
Nigel Killeen
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Street address |
513 Parnassus Avenue, Box0414
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City |
San Francisco |
State/province |
CA |
ZIP/Postal code |
94122 |
Country |
USA |
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Platforms (1) |
GPL7656 |
Mouse Exonic Evidence Based Oligonucleotide (MEEBO) spotted microarrays |
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Samples (16)
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Relations |
BioProject |
PRJNA110195 |