Opposing regulation of T cell function by Egr-1/NAB2 and Egr-2/Egr-3
TCR-induced NF-AT activation leads to the up-regulation of multiple genes involved in T cell anergy. Since NF-AT is also involved in T cell activation, we have endeavored to dissect TCR-induced activating and inhibitory genetic programs. This approach revealed roles for the early growth response (Eg...
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Published in | European journal of immunology Vol. 38; no. 2; pp. 528 - 536 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Weinheim
Wiley-VCH Verlag
01.02.2008
WILEY‐VCH Verlag |
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Abstract | TCR-induced NF-AT activation leads to the up-regulation of multiple genes involved in T cell anergy. Since NF-AT is also involved in T cell activation, we have endeavored to dissect TCR-induced activating and inhibitory genetic programs. This approach revealed roles for the early growth response (Egr) family of transcription factors and the Egr coactivator/corepressor NGFI-A-binding protein (NAB)2 in regulating T cell function. TCR-induced Egr-1 and NAB2 enhance T cell function, while Egr-2 and Egr-3 inhibit T cell function. In this report, we demonstrate that Egr-2 and Egr-3 are induced by NF-AT in the absence of AP-1, while Egr-1 and NAB2 both require AP-1-mediated transcription. Our data suggest that Egr-3 is upstream of Egr-2, and that mechanistically Egr-2 and Egr-3 suppress Egr-1 and NAB2 expression. Functionally, T cells from Egr-2 and Egr-3 null mice are hyperresponsive while T cells from Egr-3 transgenic, overexpressing mice are hyporesponsive. Furthermore, an in vivo model of autoimmune pneumonitis reveals that T cells from Egr-3 null mice hasten death while Egr-3-overexpressing T cells cause less disease. Overall, our data suggest that just as the Egr/NAB network of genes control cell fate in other systems, TCR-induced Egr-1, 2, 3 and NAB2 control the fate of antigen recognition in T cells. |
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AbstractList | TCR-induced NF-AT activation leads to the up-regulation of multiple genes involved in T cell anergy. Since NF-AT is also involved in T cell activation, we have endeavored to dissect TCR-induced activating and inhibitory genetic programs. This approach revealed roles for the early growth response (Egr) family of transcription factors and the Egr coactivator/corepressor NGFI-A-binding protein (NAB)2 in regulating T cell function. TCR-induced Egr-1 and NAB2 enhance T cell function, while Egr-2 and Egr-3 inhibit T cell function. In this report, we demonstrate that Egr-2 and Egr-3 are induced by NF-AT in the absence of AP-1, while Egr-1 and NAB2 both require AP-1-mediated transcription. Our data suggest that Egr-3 is upstream of Egr-2, and that mechanistically Egr-2 and Egr-3 suppress Egr-1 and NAB2 expression. Functionally, T cells from Egr-2 and Egr-3 null mice are hyperresponsive while T cells from Egr-3 transgenic, overexpressing mice are hyporesponsive. Furthermore, an
in vivo
model of autoimmune pneumonitis reveals that T cells from Egr-3 null mice hasten death while Egr-3-overexpressing T cells cause less disease. Overall, our data suggest that just as the Egr/NAB network of genes control cell fate in other systems, TCR-induced Egr-1, 2, 3 and NAB2 control the fate of antigen recognition in T cells. TCR‐induced NF‐AT activation leads to the up‐regulation of multiple genes involved in T cell anergy. Since NF‐AT is also involved in T cell activation, we have endeavored to dissect TCR‐induced activating and inhibitory genetic programs. This approach revealed roles for the early growth response (Egr) family of transcription factors and the Egr coactivator/corepressor NGFI‐A‐binding protein (NAB)2 in regulating T cell function. TCR‐induced Egr‐1 and NAB2 enhance T cell function, while Egr‐2 and Egr‐3 inhibit T cell function. In this report, we demonstrate that Egr‐2 and Egr‐3 are induced by NF‐AT in the absence of AP‐1, while Egr‐1 and NAB2 both require AP‐1‐mediated transcription. Our data suggest that Egr‐3 is upstream of Egr‐2, and that mechanistically Egr‐2 and Egr‐3 suppress Egr‐1 and NAB2 expression. Functionally, T cells from Egr‐2 and Egr‐3 null mice are hyperresponsive while T cells from Egr‐3 transgenic, overexpressing mice are hyporesponsive. Furthermore, an in vivo model of autoimmune pneumonitis reveals that T cells from Egr‐3 null mice hasten death while Egr‐3‐overexpressing T cells cause less disease. Overall, our data suggest that just as the Egr/NAB network of genes control cell fate in other systems, TCR‐induced Egr‐1, 2, 3 and NAB2 control the fate of antigen recognition in T cells. Abstract TCR‐induced NF‐AT activation leads to the up‐regulation of multiple genes involved in T cell anergy. Since NF‐AT is also involved in T cell activation, we have endeavored to dissect TCR‐induced activating and inhibitory genetic programs. This approach revealed roles for the early growth response (Egr) family of transcription factors and the Egr coactivator/corepressor NGFI‐A‐binding protein (NAB)2 in regulating T cell function. TCR‐induced Egr‐1 and NAB2 enhance T cell function, while Egr‐2 and Egr‐3 inhibit T cell function. In this report, we demonstrate that Egr‐2 and Egr‐3 are induced by NF‐AT in the absence of AP‐1, while Egr‐1 and NAB2 both require AP‐1‐mediated transcription. Our data suggest that Egr‐3 is upstream of Egr‐2, and that mechanistically Egr‐2 and Egr‐3 suppress Egr‐1 and NAB2 expression. Functionally, T cells from Egr‐2 and Egr‐3 null mice are hyperresponsive while T cells from Egr‐3 transgenic, overexpressing mice are hyporesponsive. Furthermore, an in vivo model of autoimmune pneumonitis reveals that T cells from Egr‐3 null mice hasten death while Egr‐3‐overexpressing T cells cause less disease. Overall, our data suggest that just as the Egr/NAB network of genes control cell fate in other systems, TCR‐induced Egr‐1, 2, 3 and NAB2 control the fate of antigen recognition in T cells. |
Author | Lutz, Michael A Anders, Robert A Zarek, Paul E Kersh, Gilbert J Collins, Sam Powell, Jonathan D |
AuthorAffiliation | 3 Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA 1 The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA 2 Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA |
AuthorAffiliation_xml | – name: 1 The Sidney Kimmel Comprehensive Cancer Center, Johns Hopkins University School of Medicine, Baltimore, MD, USA – name: 2 Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, USA – name: 3 Department of Pathology and Laboratory Medicine, Emory University School of Medicine, Atlanta, GA, USA |
Author_xml | – sequence: 1 fullname: Collins, Sam – sequence: 2 fullname: Lutz, Michael A – sequence: 3 fullname: Zarek, Paul E – sequence: 4 fullname: Anders, Robert A – sequence: 5 fullname: Kersh, Gilbert J – sequence: 6 fullname: Powell, Jonathan D |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/18203138$$D View this record in MEDLINE/PubMed |
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Snippet | TCR-induced NF-AT activation leads to the up-regulation of multiple genes involved in T cell anergy. Since NF-AT is also involved in T cell activation, we have... TCR‐induced NF‐AT activation leads to the up‐regulation of multiple genes involved in T cell anergy. Since NF‐AT is also involved in T cell activation, we have... Abstract TCR‐induced NF‐AT activation leads to the up‐regulation of multiple genes involved in T cell anergy. Since NF‐AT is also involved in T cell... |
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SubjectTerms | Activation Animals Early Growth Response Protein 1 - antagonists & inhibitors Early Growth Response Protein 1 - biosynthesis Early Growth Response Protein 1 - genetics Early Growth Response Protein 1 - physiology Early Growth Response Protein 2 - biosynthesis Early Growth Response Protein 2 - deficiency Early Growth Response Protein 2 - genetics Early Growth Response Protein 2 - physiology Early Growth Response Protein 3 - biosynthesis Early Growth Response Protein 3 - deficiency Early Growth Response Protein 3 - genetics Early Growth Response Protein 3 - physiology EGR Gene Expression Regulation - immunology Mice Mice, Inbred BALB C Mice, Inbred C57BL Mice, Knockout Mice, Transgenic NAB2 Neoplasm Proteins - antagonists & inhibitors Neoplasm Proteins - biosynthesis Neoplasm Proteins - genetics Neoplasm Proteins - physiology Receptors, Antigen, T-Cell - physiology Repressor Proteins - antagonists & inhibitors Repressor Proteins - biosynthesis Repressor Proteins - genetics Repressor Proteins - physiology T cells T-Lymphocytes - immunology T-Lymphocytes - metabolism Tolerance |
Title | Opposing regulation of T cell function by Egr-1/NAB2 and Egr-2/Egr-3 |
URI | https://onlinelibrary.wiley.com/doi/abs/10.1002%2Feji.200737157 https://www.ncbi.nlm.nih.gov/pubmed/18203138 https://search.proquest.com/docview/70260983 https://pubmed.ncbi.nlm.nih.gov/PMC3598016 |
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