NDLI: STAT4 isoforms differentially regulate Th1 cytokine production and the severity of inflammatory bowel disease.

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STAT4 isoforms differentially regulate Th1 cytokine production and the severity of inflammatory bowel disease.

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Year: 2008 Volume: 181 Issue: 6

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Year: 2008 Volume: 181 Issue: 3

Year: 2008 Volume: 181 Issue: 2

STAT4 isoforms differentially regulate Th1 cytokine production and the severity of inflammatory bowel disease.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Chang, Hua-Chen Srinivasan, Mythily Kaplan, Mark H. Hogenesch, Harm Stritesky, Gretta L. Eri, Rajaraman D. O'Malley, John T. Mathur, Anubhav N.
Description	Country affiliation: United States Author Affiliation: O'Malley JT ( Department of Pediatrics, HB Wells Center for Pediatric Research and Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202, USA.)
Abstract	STAT4, a critical regulator of inflammation in vivo, can be expressed as two alternative splice forms, a full-length STAT4alpha, and a STAT4beta isoform lacking a C-terminal transactivation domain. Each isoform is sufficient to program Th1 development through both common and distinct subsets of target genes. However, the ability of these isoforms to mediate inflammation in vivo has not been examined. Using a model of colitis that develops following transfer of CD4(+) CD45RB(high) T cells expressing either the STAT4alpha or STAT4beta isoform into SCID mice, we determined that although both isoforms mediate inflammation and weight loss, STAT4beta promotes greater colonic inflammation and tissue destruction. This correlates with STAT4 isoform-dependent expression of TNF-alpha and GM-CSF in vitro and in vivo, but not Th1 expression of IFN-gamma or Th17 expression of IL-17, which were similar in STAT4alpha- and STAT4beta-expressing T cells. Thus, higher expression of a subset of inflammatory cytokines from STAT4beta-expressing T cells correlates with the ability of STAT4beta-expressing T cells to mediate more severe inflammatory disease.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	7
Volume Number	181
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2008-10-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cytokines Biosynthesis Inflammation Mediators Physiology Inflammatory Bowel Diseases Immunology Pathology Stat4 Transcription Factor Severity Of Illness Index Th1 Cells Animals Cells, Cultured Metabolism Genetics Lymphocyte Transfusion Mice Mice, Inbred C57bl Mice, Knockout Mice, Scid Mice, Transgenic Protein Isoforms Deficiency Protein Structure, Tertiary Receptors, Antigen, T-cell Sequence Deletion Secretion Transplantation Transcriptional Activation Tumor Necrosis Factor-alpha Up-regulation Weight Loss Comparative Study Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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