Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2004-9-9
pubmed:abstractText
Previous in vitro work has implicated a role for transcriptional factor early growth response gene 1 (EGR1) in regulating immune responses. However, the in vivo role of EGR1 in orchestrating T cell responses has not been studied. To investigate the importance of EGR1 in T cell immunity, we compared Ag-specific CD8 T cell responses between wild type (+/+) and EGR1-deficient (EGR1-/-) mice following an acute infection with lymphocytic choriomeningitis virus (LCMV). These studies revealed that the expansion of LCMV-specific CD8 T cells was substantially reduced in EGR1-/- mice, as compared with +/+ mice. The reduced numbers of LCMV-specific CD8 T cells in EGR1-/- mice were not due to an intrinsic T cell defect per se because purified EGR1-deficient T cells exhibited normal proliferative response to anti-CD3 stimulation in vitro, and underwent normal activation and expansion in response to LCMV upon adoptive transfer into T cell-deficient mice. Furthermore, adoptive transfer of CD8 T cells bearing a transgenic TCR into EGR1-/- mice showed that EGR1 deficiency in non-CD8 T cells impaired CD8 T cell expansion in vivo following an LCMV infection. Further investigations on accessory cells showed that bone marrow-derived dendritic cells from EGR1-/- mice did not exhibit detectable impairment to prime Ag-specific CD8 T cell responses in vivo. However, in LCMV-infected mice, EGR1 deficiency selectively impaired the maturation of CD8alpha(+ve) plasmacytoid dendritic cells. Taken together, our findings suggest that EGR1 might promote expansion of CD8 T cells during an acute viral infection by modulating the cues in the lymphoid microenvironment.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-1767
pubmed:author
pubmed:copyrightInfo
Copyright 2004 The American Association of Immunologists, Inc.
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
173
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3855-62
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:15356133-Acute Disease, pubmed-meshheading:15356133-Adoptive Transfer, pubmed-meshheading:15356133-Animals, pubmed-meshheading:15356133-CD8-Positive T-Lymphocytes, pubmed-meshheading:15356133-Cell Division, pubmed-meshheading:15356133-Cells, Cultured, pubmed-meshheading:15356133-DNA-Binding Proteins, pubmed-meshheading:15356133-Dendritic Cells, pubmed-meshheading:15356133-Early Growth Response Protein 1, pubmed-meshheading:15356133-Epitopes, T-Lymphocyte, pubmed-meshheading:15356133-Immediate-Early Proteins, pubmed-meshheading:15356133-Lymphocyte Activation, pubmed-meshheading:15356133-Lymphocyte Count, pubmed-meshheading:15356133-Lymphocytic Choriomeningitis, pubmed-meshheading:15356133-Lymphocytic choriomeningitis virus, pubmed-meshheading:15356133-Macrophages, pubmed-meshheading:15356133-Mice, pubmed-meshheading:15356133-Mice, Inbred C57BL, pubmed-meshheading:15356133-Mice, Knockout, pubmed-meshheading:15356133-Mice, Transgenic, pubmed-meshheading:15356133-Transcription Factors
pubmed:year
2004
pubmed:articleTitle
CD8 T cell responses to lymphocytic choriomeningitis virus in early growth response gene 1-deficient mice.
pubmed:affiliation
Department of Pathobiological Sciences, University of Wisconsin, Madison, WI 53706, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't