NDLI: Posttranscriptional modulation of cytokine production in T cells for the regulation of excessive inflammation by TFL.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wakahashi, Kanako Fukui, Chie Asada, Noboru Katayama, Yoshio Minagawa, Kentaro Kawano, Yuko Kawano, Hiroki Nishikawa, Shinichiro Sato, Mari Sada, Akiko Matsui, Toshimitsu
Description	Country affiliation: Japan Author Affiliation: Minagawa K ( Division of Hematology, Department of Medicine, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan.)
Abstract	Posttranscriptional machinery regulates inflammation and is associated with autoimmunity as well as tumorigenesis in collaboration with transcription factors. We previously identified the tumor suppressor gene transformed follicular lymphoma (TFL) on 6q25 in a patient with follicular lymphoma, which transformed into diffuse large B cell lymphoma. TFL families have a common RNase domain that governs macrophage-mediated inflammation. In human peripheral blood, TFL is dominantly expressed at the glycine- and tryptophan-rich cytoplasmic processing bodies of T lymphocytes, and it is persistently upregulated in activated T cells. To address its physiological role, we established TFL(-/-) mice in which TFL(-/-) lymphocytes proliferated more rapidly than TFL(+/+) upon stimulation with inappropriate cytokine secretion, including IL-2, IL-6, and IL-10. Moreover, TFL inhibited the synthesis of cytokines such as IL-2, IL-6, IL-10, TNF- , and IL-17a by 3' untranslated region RNA degradation. Experimental autoimmune encephalitis induced in TFL(-/-) mice demonstrated persistent severe paralysis. CNS-infiltrated CD4(+) T cells in TFL(-/-) mice contained a higher proportion of Th17 cells than did those in TFL(+/+) mice during the resolution phase, and IL-17a mRNA levels were markedly increased in TFL(-/-) cells. These results suggest that TFL may play an important role in attenuating local inflammation by suppressing the infiltration of Th17 cells in the CNS during the resolution phase of experimental autoimmune encephalitis. TFL is a novel gradual and persistent posttranscriptional regulator, and the TFL-driven attenuation of excessive inflammation could contribute to recovery from T cell-mediated autoimmune diseases.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	4
Volume Number	192
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-02-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Central Nervous System Immunology Cytokines Genetics Encephalomyelitis, Autoimmune, Experimental Gene Expression Regulation Inflammation Th17 Cells Tumor Suppressor Proteins Physiology Animals Cell Movement Cell Proliferation Pathology Interleukin-10 Biosynthesis Metabolism Interleukin-17 Interleukin-2 Interleukin-6 Lymphocyte Activation Lymphocyte Count Lymphoma, Follicular Mice Mice, Inbred C57bl Mice, Knockout Rna Processing, Post-transcriptional Ribonucleases Tumor Necrosis Factor-alpha Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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