Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2009-2-6
pubmed:abstractText
The identification of novel factors regulating human T helper (Th)-cell differentiation into functionally distinct Th1 and Th2 subsets is important for understanding the mechanisms behind human autoimmune and allergic diseases. We have identified a protein of relevant evolutionary and lymphoid interest (PRELI), a novel protein that induces oxidative stress and a mitochondrial apoptosis pathway in human primary Th cells. We also demonstrated that PRELI inhibits Th2-cell development and down-regulates signal transducer and activator of transcription 6 (STAT6), a key transcription factor driving Th2 differentiation. Our data suggest that calpain, an oxidative stress-induced cysteine protease, is involved in the PRELI-induced down-regulation of STAT6. Moreover, we observed that a strong T-cell receptor (TCR) stimulus induces expression of PRELI and inhibits Th2 development. Our results suggest that PRELI is involved in a mechanism wherein the strength of the TCR stimulus influences the polarization of Th cells. This study identifies PRELI as a novel factor influencing the human primary Th-cell death and differentiation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1528-0020
pubmed:author
pubmed:issnType
Electronic
pubmed:day
5
pubmed:volume
113
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1268-77
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:18945965-Apoptosis, pubmed-meshheading:18945965-Blotting, Western, pubmed-meshheading:18945965-Calpain, pubmed-meshheading:18945965-Cell Differentiation, pubmed-meshheading:18945965-Cells, Cultured, pubmed-meshheading:18945965-Cytokines, pubmed-meshheading:18945965-Fetal Blood, pubmed-meshheading:18945965-Fluorescent Antibody Technique, pubmed-meshheading:18945965-Gene Expression Profiling, pubmed-meshheading:18945965-Humans, pubmed-meshheading:18945965-Infant, Newborn, pubmed-meshheading:18945965-Kidney, pubmed-meshheading:18945965-Lymphocyte Activation, pubmed-meshheading:18945965-Membrane Potential, Mitochondrial, pubmed-meshheading:18945965-Mitochondria, pubmed-meshheading:18945965-Mitochondrial Proteins, pubmed-meshheading:18945965-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:18945965-Oxidative Stress, pubmed-meshheading:18945965-Proteins, pubmed-meshheading:18945965-RNA, Messenger, pubmed-meshheading:18945965-Reactive Oxygen Species, pubmed-meshheading:18945965-Receptors, Antigen, T-Cell, pubmed-meshheading:18945965-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:18945965-STAT6 Transcription Factor, pubmed-meshheading:18945965-Signal Transduction, pubmed-meshheading:18945965-Th1 Cells, pubmed-meshheading:18945965-Th2 Cells
pubmed:year
2009
pubmed:articleTitle
PRELI is a mitochondrial regulator of human primary T-helper cell apoptosis, STAT6, and Th2-cell differentiation.
pubmed:affiliation
Turku Centre for Biotechnology, University of Turku and Abo Akademi, Turku, Finland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't