NDLI: HSF1 is activated as a consequence of lymphocyte activation and regulates a major proteostasis network in T cells critical for cell division during stress

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HSF1 is activated as a consequence of lymphocyte activation and regulates a major proteostasis network in T cells critical for cell division during stress

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Gandhapudi, Siva K. Woodward, Jerold G. Sarge, Kevin D. Snow, Charles Threlkeld, Zachary D. Ward, Martin Murapa, Patience
Description	Author Affiliation: Gandhapudi SK ( Department of Microbiology, Immunology and Molecular Genetics, University of Kentucky School of Medicine, Lexington, KY 40536.)
Abstract	Heat shock transcription factor 1 (HSF1) is a major transcriptional regulator of the heat shock response in eukaryotic cells. HSF1 is evoked in response to a variety of cellular stressors, including elevated temperatures, oxidative stress, and other proteotoxic stressors. Previously, we demonstrated that HSF1 is activated in naive T cells at fever range temperatures (39.5°C) and is critical for in vitro T cell proliferation at fever temperatures. In this study, we demonstrated that murine HSF1 became activated to the DNA-binding form and transactivated a large number of genes in lymphoid cells strictly as a consequence of receptor activation in the absence of apparent cellular stress. Microarray analysis comparing HSF1(+/+) and HSF1(-/-) gene expression in T cells activated at 37°C revealed a diverse set of 323 genes significantly regulated by HSF1 in nonstressed T cells. In vivo proliferation studies revealed a significant impairment of HSF1(-/-) T cell expansion under conditions mimicking a robust immune response (staphylococcal enterotoxin B-induced T cell activation). This proliferation defect due to loss of HSF1 is observed even under nonfebrile temperatures. HSF1(-/-) T cells activated at fever temperatures show a dramatic reduction in cyclin E and cyclin A proteins during the cell cycle, although the transcription of these genes was modestly affected. Finally, B cell and hematopoietic stem cell proliferation from HSF1(-/-) mice, but not HSF1(+/+) mice, were also attenuated under stressful conditions, indicating that HSF1 is critical for the cell cycle progression of lymphoid cells activated under stressful conditions.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1202831
Journal	The Journal of Immunology
Issue Number	8
Volume Number	191
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-10-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Dna-binding Proteins Metabolism Lymphocyte Activation Stress, Physiological T-lymphocytes Immunology Transcription Factors Animals Cell Cycle Cell Division Cell Proliferation Cells, Cultured Cyclin A Biosynthesis Cyclin E Genetics Enterotoxins Fever Gene Expression Regulation Heat-shock Proteins Heat-shock Response Mice Mice, Inbred Balb C Mice, Knockout Reactive Oxygen Species Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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HSF1 is activated as a consequence of lymphocyte activation and regulates a major proteostasis network in T cells critical for cell division during stress