T cell activation induces a noncoding RNA transcript sensitive to inhibition by immunosuppressant drugs and encoded by the proto-oncogene, BIC

Haasch, Deanna L.; Chen, Yung-Wu; Reilly, Regina M.; Chiou, X. Grace; Koterski, Sandra; Smith, Morey L.; Kroeger, Paul E.; McWeeny, Kerri; Halbert, Donald N.; Mollison, Karl W.; Djurić, Stevan W.; Trevillyan, James M.

doi:10.1016/s0008-8749(02)00506-3

Cited by 172 publications

(131 citation statements)

References 34 publications

Supporting

Mentioning

124

Contrasting

Unclassified

Order By: Relevance

“…Under normal conditions, miR-155 has been described to be expressed by human T cells, B cells, monocytes, and endothelial cells (29,(31)(32)(33). Under pathologic conditions, miR-155 has been associated with a number of human neoplastic disorders.…”

Section: Discussionmentioning

confidence: 99%

Altered expression of MicroRNA in synovial fibroblasts and synovial tissue in rheumatoid arthritis

Stańczyk

Pedrioli

Brentano

et al. 2008

Arthritis & Rheumatism

756

624

View full text Add to dashboard Cite

Objective. MicroRNAs (miRNA) have recently emerged as a new class of modulators of gene expression. In this study we investigated the expression, regulation, and function of miR-155 and miR-146a in rheumatoid arthritis (RA) synovial fibroblasts (RASFs) and RA synovial tissue.Methods. Locked nucleic acid microarray was used to screen for differentially expressed miRNA in RASFs treated with tumor necrosis factor ␣ (TNF␣). TaqMan-based real-time polymerase chain reaction was applied to measure the levels of miR-155 and miR-146a. Enforced overexpression of miR-155 was used to investigate the function of miR-155 in RASFs.Results

show abstract

Section: Discussionmentioning

confidence: 99%

Altered expression of MicroRNA in synovial fibroblasts and synovial tissue in rheumatoid arthritis

Stańczyk

Pedrioli

Brentano

et al. 2008

Arthritis & Rheumatism

756

624

View full text Add to dashboard Cite

show abstract

“…Mir-155 was among the first miRNAs identified as operating in T cells, and its expression has been linked to activation following TCR stimulation (41,42). Mice deficient in miR-155 develop an increased inflammatory remodeling of lung airways, reminiscent of autoimmune-mediated lung fibrosis and enteric inflammation (16).…”

Section: Discussionmentioning

confidence: 99%

microRNA-301a regulation of a T-helper 17 immune response controls autoimmune demyelination

Mycko

Cichalewska²,

Machlańska³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

179

143

View full text Add to dashboard Cite

MicroRNAs (miRNAs) are an emerging group of short, noncoding RNAs that play an important role in regulating expression of classical genes. Thus far little is known about their role in autoimmune demyelination. In this study, we analyzed changes in the miRNA profile in CD4 + T cells that occurred during the recognition of the myelin autoantigen, MOG . We found that, both in vivo and in vitro, myelin antigen stimulation resulted in significant up-regulation of miR-301a, miR-21, and miR-155. Furthermore, these three miRNAs were overexpressed in T cells infiltrating the CNS in animals with experimental autoimmune encephalomyelitis. Use of specific miRNA antagonists, antagomirs, revealed that miR-301a contributed to the development of the T-helper type 17 subset via targeting the IL-6/23-STAT3 pathway. This contribution appeared to be mediated by the miR-301a effect on the expression of the PIAS3, a potent inhibitor of the STAT3 pathway. Manipulation of miR-301a levels or PIAS3 expression in myelin-specific CD4 + T cells led to significant changes in the severity of experimental autoimmune encephalomyelitis. Thus, we have identified a role of miR-301a in regulating the function of myelinreactive T-helper type 17 cells, supporting a role for miR-301a and PIAS3 as candidates for therapeutic targets for controlling of autoimmune demyelination.M ultiple sclerosis (MS) is an organ-specific autoimmune disease manifested by chronic inflammatory demyelination of the CNS. CD4 + T-cell-mediated autoimmunity, with a critical role of a putative myelin autoantigen, has long been accepted as one of the most important aspects of MS pathogenesis, especially for the early initiation of disease (1). This understanding has been particularly complemented by the research on the MS animal model, experimental autoimmune encephalomyelitis (EAE). T-helper type 1 (Th1) cells, characterized by the expression of the transcription factor T-bet and the production of IFN-γ, originally were considered the major effector T-helper cells that mediate the pathogenesis of autoimmune demyelination (2). More recently another subset of T-helper cells, Th17, characterized by expression of the transcription factors retinoic acid receptor-related orphan receptor alpha (ROR-α) and retinoic acid receptor-related orphan receptor gamma t (ROR-γt) and by the production of IL-17, has been considered pivotal for the propagation of autoimmune demyelination (3). Mice with impaired numbers or function of Th17 cells, particularly mice deficient in the cytokines IL-6 or IL-23, are largely resistant to EAE (4-6). However, precise mechanisms governing the development and function of Th17 cells resulting in autoimmune demyelination are still unclear. Thus, Th17-targeting therapeutic approaches for MS have not yet been established.MicroRNAs (miRNAs) have begun to emerge as an important component in the differentiation and function of cells involved in the immune response. miRNAs operate as noncoding RNA molecules ∼22 nt in length that are processed from larger transcripts o...

show abstract

“…20 This induction could be blocked by calcineurin blockers like cyclosporin A or FK506. The data suggest an association between activation of B and T cells and induction of high BIC/miR-155 levels.…”

Section: Mir-155mentioning

confidence: 99%

The role of microRNAs in normal hematopoiesis and hematopoietic malignancies

et al. 2006

View full text Add to dashboard Cite

T cell activation induces a noncoding RNA transcript sensitive to inhibition by immunosuppressant drugs and encoded by the proto-oncogene, BIC

Cited by 172 publications

References 34 publications

Altered expression of MicroRNA in synovial fibroblasts and synovial tissue in rheumatoid arthritis

Altered expression of MicroRNA in synovial fibroblasts and synovial tissue in rheumatoid arthritis

microRNA-301a regulation of a T-helper 17 immune response controls autoimmune demyelination

The role of microRNAs in normal hematopoiesis and hematopoietic malignancies

Contact Info

Product

Resources

About