Targeting TNF superfamily members for therapeutic intervention in rheumatoid arthritis

Vinay, Dass S.; Kwon, Byoung S.

doi:10.1016/j.cyto.2011.12.005

Cited by 28 publications

(16 citation statements)

References 150 publications

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“…Anti-TNF antibodies are an effective therapy for various inflammatory conditions such as rheumatoid arthritis (Vinay and Kwon 2012) and inflammatory bowel disease (Hering and Schulzke 2009). The use of anti-TNF therapy in CF is not routine, and in fact there are only three case reports in the literature.…”

Section: Discussionmentioning

confidence: 99%

Disrupted tight junctions in the small intestine of cystic fibrosis mice

Lisle

2013

Cell Tissue Res

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The tight junction (TJ) is the major determinant of paracellular permeability, which in the gut protects the body from entry of harmful substances such as microbial components. In cystic fibrosis (CF) there is increased permeability of the small intestine both in humans and in CF mice. To gain insight into the mechanisms of increased intestinal permeability in CF, I analyzed the composition of the TJ in the cystic fibrosis transmembrane conductance regulator (Cftr) knockout mouse model. Significant changes in TJ gene expression in the CF intestine were found for Cldn1, Cldn7, Cldn8, and Pmp22 which were expressed at lower levels; and Cldn2 which was expressed at a higher level. Protein levels of claudin-2 were increased in the CF intestine as compared to wild type, while other TJ proteins were not significantly different. In the villus epithelium of the CF intestine, all TJ components analyzed were mislocalized to the basal cytoplasm and showed varying degrees of loss from the TJ and apico-lateral surfaces. The pore-forming claudin-2 in the CF intestine showed more intense staining but was correctly localized to the TJ, principally in the crypts which are enlarged in CF. The cytokine TNFα, known to affect TJ, was elevated to 160% of wild type in the CF intestine. In summary, there is a dramatic redistribution of claudin proteins from the TJ/lateral membrane to the basal cytoplasm of the villus epithelium in the CF intestine. These changes in TJ protein localization in CF are likely to be involved in the increased permeability of the CF small intestine to macromolecules, and TNFα may be a causative factor.

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Section: Discussionmentioning

confidence: 99%

Disrupted tight junctions in the small intestine of cystic fibrosis mice

Lisle

2013

Cell Tissue Res

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“…Rheumatoid arthritis (RA) is an autoimmune disease characterized by synovial hyperplasia and inflammatory cell recruitment eventually leading to destruction of cartilage and bone [1], [2]. It afflicts approximately 1% of the worldwide population [3].…”

Section: Introductionmentioning

confidence: 99%

Glycyrol Suppresses Collagen-Induced Arthritis by Regulating Autoimmune and Inflammatory Responses

Zhou

Wang

et al. 2014

PLoS ONE

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Glycyrol is a natural compound extracted from Glycyrrhiza uralensis, first reported by us to be a new immunosuppressant. Here, we demonstrate its beneficial effect in collagen-induced arthritis (CIA) in mice, a model for rheumatoid arthritis (RA) in man, and we document the underlying mechanisms. Peroral administration of glycyrol significantly reduced clinical scores, alleviated cartilage and bone erosion and reduced levels of serum inflammatory cytokines. Glycyrol also decreased delayed-type hypersensitivity, improved carbon clearance and reduced acetic acid-induced capillary permeability. Furthermore, glycyrol decreased NF-κB and NFAT transcriptional activities and inhibited IL-2 expression. The therapeutic effect of glycyrol was associated with down-regulation of both autoimmune and inflammatory reactions. In addition, we demonstrated that glycyrol has minimal acute toxicity in mice. Therefore, we propose that glycyrol may hold promise for future treatment of RA.

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“…Rheumatoid arthritis (RA) is a common, chronic, systemic, and inflammatory autoimmune disorder that primarily affects the small diarthrodial joints of the hands and feet, affecting approximately 1% of the world's population [1–3]. The main characteristics of this disease are synovium hyperplasia, lymphocyte infiltration, and the abnormal proliferation of fibroblast-like synoviocytes (FLS) that can lead to the destruction of bone and cartilage and eventual disability [4].…”

Section: Introductionmentioning

confidence: 99%

Alternative Expression Pattern of MALT1-A20-NF-κB in Patients with Rheumatoid Arthritis

Wang

Zhu

Liao

et al. 2014

Journal of Immunology Research

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Rheumatoid arthritis (RA) is an inflammatory autoimmune disorder; abnormal T cell immunity plays a critical role in the development of RA. Recently, A20 was identified as a key negative regulator for T cell activation and inflammatory signaling and may be involved in RA pathogenesis. In this study, we analyzed the expression level of A20, NF-κB, and A20 regulatory factor mucosa-associated lymphoid tissue lymphoma translocation gene 1 (MALT1) in patients with RA. Real-time PCR was used to determine the expression level of MALT1, MALT-V1, A20, and NF-κB genes in RA and healthy individuals (HI). Significantly lower A20 expression was found in RA patients compared with those in the healthy group, while NF-κB overexpression could be detected in patients with RA. Moreover, the MALT1 and MALT1-V1 expression level was downregulated in RA patients. A positive correlation between MALT1 and A20 and MALT1-V1 and A20 was found in patients with RA, and a tendency towards a negative correlation was found between MALT1 and NF-κB, MALT1-V1 and NF-κB, and A20 and NF-κB. In conclusion, we first characterized the alternative expression pattern of MALT1, A20, and NF-κB in RA, which may be related to abnormal T cell activation.

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Targeting TNF superfamily members for therapeutic intervention in rheumatoid arthritis

Cited by 28 publications

References 150 publications

Disrupted tight junctions in the small intestine of cystic fibrosis mice

Disrupted tight junctions in the small intestine of cystic fibrosis mice

Glycyrol Suppresses Collagen-Induced Arthritis by Regulating Autoimmune and Inflammatory Responses

Alternative Expression Pattern of MALT1-A20-NF-κB in Patients with Rheumatoid Arthritis

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