Expression of human TIM-3 and its correlation with disease activity in rheumatoid arthritis

J, Lee; Jm, Oh; Jw, Hwang; Jk, Ahn; Ek, Bae; Won, Jonghwa; Em, Koh; Hs, Cha

doi:10.3109/03009742.2010.547871

Cited by 47 publications

(41 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The current study measured Tim-3 expression in FLS from patients with RA using western blot analysis and RT-PCR. Consistent with previous studies (18,19), the results of the present study demonstrated that Tim-3 expression in FLS from patients with RA was significantly higher than that of controls. Specific siRNA was designed to decrease Tim-3 expression.…”

Section: Discussionsupporting

confidence: 93%

“…Tim-3 is considered to be a specific surface marker of Th1 cells and is able to regulate the immune response of Th1 cells to participate in systemic lupus erythematosus, aplastic anemia and other autoimmune diseases (16,17). Furthermore, Tim-3 is highly expressed in cluster of differentiation (CD)4 + T cells, as well as the synovial tissue of patients with RA (17)(18)(19). Tim-3 is closely associated with the TLR4 signaling pathway and participates in a variety of immune diseases by regulating this signaling pathway (20,21).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of Tim-3 silencing on the viability of fibroblast-like synoviocytes and lipopolysaccharide-induced inflammatory reactions

Long

Chen

et al. 2017

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

Abstract. The objective of the present study was to investigate the effects of Tim-3 silencing on cell viability and lipopolysaccharide (LPS)-induced inflammatory reactions in fibroblast-like synoviocytes (FLS). T-cell immunoglobulin mucin domain molecule (Tim)-3 expression in FLS obtained from patients with rheumatoid arthritis (RA) and normal controls were detected by western blot analysis and reverse transcription-polymerase chain reaction (RT-PCR). Small interfering (si)RNA was transfected using Lipofectamine ® 2000 to decrease Tim-3 expression. Following transfection, FLS were stimulated by LPS. An MTT assay, RT-PCR and western blot analysis were performed to measure cell viability, Toll-like receptor 4 (TLR4) signaling pathway-related protein expression and inflammatory cytokine release, respectively. The results of the present study indicated that Tim-3 expression was increased in FLS from patients with RA compared with FLS from healthy controls. Transfection of Tim-3 siRNA significantly decreased Tim-3 expression in FLS from patients with RA. Notably, Tim-3 silencing decreased FLS cell viability. Following stimulation with LPS, cell viability and the expression of TLR4, myeloid differentiation protein gene 88 (MyD88) and nuclear factor-κB (NF-κB) p65 were enhanced in FLS. By contrast, Tim-3 silencing attenuated LPS-induced cell proliferation and the expression of TLR4, MyD88 and NF-κB p65. In addition, LPS significantly increased levels of cytokines in the supernatant, including tumor necrosis factor-α, interferon-γ and interleukin-6 (P<0.01). By contrast, Tim-3 silencing significantly decreased LPS-induced cytokine release (P<0.01). However, Tim-3 silencing did not affect TLR4, MyD88 and NF-κB p65 expression and the release of cytokines in cells that did not undergo treatment with LPS. Therefore, the results of the present study indicate that Tim-3 silencing decreases the viability of FLS in RA and attenuates the LPS-induced inflammatory reaction.

show abstract

Section: Discussionsupporting

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Effects of Tim-3 silencing on the viability of fibroblast-like synoviocytes and lipopolysaccharide-induced inflammatory reactions

Long

Chen

et al. 2017

Experimental and Therapeutic Medicine

View full text Add to dashboard Cite

show abstract

“…Dysregulation of TIM3 expression in CD4+ T cells has been recently revealed in autoimmune diseases such as rheumatoid arthritis and multiple sclerosis (Lee et al, 2011;Liu et al, 2010;Yang et al, 2008). Therefore, identification of the regulatory molecules for TIM3 expression may have implications in understanding pathogenesis of such diseases as well as normal immune responses in which TIM3 exerts its control against excessive TH1 immune response.…”

Section: Discussionmentioning

confidence: 99%

Activation of mitogen activated protein kinase-Erk kinase (MEK) increases T cell immunoglobulin mucin domain-3 (TIM-3) transcription in human T lymphocytes and a human mast cell line

Yoon

Lee

Shin

et al. 2011

Molecular Immunology

View full text Add to dashboard Cite

“…T-cell immunoglobulin mucin-3 (TIM-3) [74] is another proapoptosis-related protein that may become a target for intervention in human RA. In that regard, Lee et al [75] showed that TIM-3 expression was lower in RA CD4 + T-cells compared to CD4 + T-cells from normal subjects.…”

Section: Bh3-only Proteinsmentioning

confidence: 99%

Apoptosis Resistance in Rheumatoid Arthritis Synovial Tissue

Malemud¹

2012

J Clin Cell Immunol

View full text Add to dashboard Cite

Expression of human TIM-3 and its correlation with disease activity in rheumatoid arthritis

Cited by 47 publications

References 26 publications

Effects of Tim-3 silencing on the viability of fibroblast-like synoviocytes and lipopolysaccharide-induced inflammatory reactions

Effects of Tim-3 silencing on the viability of fibroblast-like synoviocytes and lipopolysaccharide-induced inflammatory reactions

Activation of mitogen activated protein kinase-Erk kinase (MEK) increases T cell immunoglobulin mucin domain-3 (TIM-3) transcription in human T lymphocytes and a human mast cell line

Apoptosis Resistance in Rheumatoid Arthritis Synovial Tissue

Contact Info

Product

Resources

About