Local microbleeding facilitates IL-6– and IL-17–dependent arthritis in the absence of tissue antigen recognition by activated T cells

Murakami, Masaaki; Okuyama, Yuko; Ogura, Hideki; Asano, Shogo; Arima, Yasunobu; Tsuruoka, Mineko; Harada, Masaya; Kanamoto, Minoru; Sawa, Yukihisa; Iwakura, Yoichiro; Takatsu, Kiyoshi; Kamimura, Daisuke; Hirano, Toshio

doi:10.1084/jem.2010090020912c

Cited by 19 publications

(30 citation statements)

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“…1f). These findings suggest that under arthritic conditions, CD25 lo Foxp3 + CD4 + T cells are prone to differentiate into T H 17 cells that are known to have a key pathological role in arthritis [13][14][15][16][17][18] .…”

Section: Results T H 17 Cells Arise From Cd25 Lo Foxp3 + T Cells In Amentioning

confidence: 93%

Pathogenic conversion of Foxp3+ T cells into TH17 cells in autoimmune arthritis

Komatsu

Okamoto

Sawa

et al. 2013

Nat Med

944

781

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Section: Results T H 17 Cells Arise From Cd25 Lo Foxp3 + T Cells In Amentioning

confidence: 93%

Pathogenic conversion of Foxp3+ T cells into TH17 cells in autoimmune arthritis

Komatsu

Okamoto

Sawa

et al. 2013

Nat Med

944

781

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“…F759 mice were backcrossed with C57BL/6 mice for .10 generations (20). All mice were maintained under specific pathogen-free conditions according to the protocols of Osaka and Hokkaido Universities.…”

Section: Methodsmentioning

confidence: 99%

“…Mice were inspected and assessed for signs of arthritis as described previously (20). Joints were injected with a lentivirus carrying short hairpin RNA (shRNA) specific for BCR (Sigma-Aldrich) or a lentivirus carrying a scrambled sequence (Sigma-Aldrich).…”

Section: Clinical Assessment Of Arthritismentioning

confidence: 99%

“…IL-6 and IL-17 (100 ng each) were injected at the ankle joints of F759 mice on days 0, 1, and 2 to induce cytokine-induced arthritis, as described previously (17,19,20). On day 7, the ankle joints were harvested, and paraffin sections were prepared after formalin fixation and decalcification.…”

Section: Immunohistochemistry Experimentsmentioning

confidence: 99%

“…These results demonstrated that BCR is critical for NF-kB activation in nonimmune cells after cytokine stimulation. We next investigated whether BCR-mediated NF-kB activation is critical for a rheumatoid arthritis model (20). BCR shRNA in the joints suppressed the development of arthritis (Fig.…”

Section: Bcr Is Critical For Nf-kb Activation In Vivo and In Vitromentioning

confidence: 99%

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Breakpoint Cluster Region–Mediated Inflammation Is Dependent on Casein Kinase II

Meng

Jiang

Atsumi

et al. 2016

The Journal of Immunology

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The breakpoint cluster region (BCR) is known as a kinase and cause of leukemia upon fusing to Abl kinase. In this study, we demonstrate that BCR associated with the α subunit of casein kinase II (CK2α), rather than BCR itself, is required for inflammation development. We found that BCR knockdown inhibited NF-κB activation in vitro and in vivo. Computer simulation, however, suggested that the putative BCR kinase domain has an unstable structure with minimal enzymatic activity. Liquid chromatography–tandem mass spectrometry analysis showed that CK2α associated with BCR. We found the BCR functions are mediated by CK2α. Indeed, CK2α associated with adaptor molecules of TNF-αR and phosphorylated BCR at Y177 to establish a p65 binding site after TNF-α stimulation. Notably, p65 S529 phosphorylation by CK2α creates a p300 binding site and increased p65-mediated transcription followed by inflammation development in vivo. These results suggest that BCR-mediated inflammation is dependent on CK2α, and the BCR–CK2α complex could be a novel therapeutic target for various inflammatory diseases.

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Intermittent hypoxia‐induced epiregulin expression by IL‐6 production in human coronary artery smooth muscle cells

et al. 2018

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Patients with obstructive sleep apnea ( OSA ) experience repetitive episodes of desaturation and resaturation of blood oxygen (known as intermittent hypoxia or IH ), during sleep. We showed previously that IH induced excessive proliferation of rat vascular smooth muscle cells through upregulation of members of the epidermal growth factor family, especially epiregulin ( EREG ), and the erbB2 receptor. In this study, we exposed human coronary artery smooth muscle cells to IH and found that IH significantly increased the expression of EREG . IH increased the production of interleukin‐6 ( IL ‐6) in smooth muscle cells, and the addition of IL ‐6 induced EREG expression. Small interfering RNA for IL ‐6 or IL ‐6 receptor attenuated the IH ‐induced increase in EREG . IL ‐6 may play a pivotal role in EREG upregulation by IH and consequently OSA ‐related atherosclerosis.

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Local microbleeding facilitates IL-6– and IL-17–dependent arthritis in the absence of tissue antigen recognition by activated T cells

Cited by 19 publications

References 0 publications

Pathogenic conversion of Foxp3+ T cells into TH17 cells in autoimmune arthritis

Pathogenic conversion of Foxp3+ T cells into TH17 cells in autoimmune arthritis

Breakpoint Cluster Region–Mediated Inflammation Is Dependent on Casein Kinase II

Intermittent hypoxia‐induced epiregulin expression by IL‐6 production in human coronary artery smooth muscle cells

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