Casein Kinase II exacerbates rheumatoid arthritis via promoting Th1 and Th17 cell inflammatory responses

Ye, Hua; Fu, Dongdong; Fang, Xiangyu; Xie, Yang; Zheng, Xi; Fan, Wenqiang; Hu, Fanlei; Li, Zhanguo

doi:10.1080/14728222.2021.2010190

Cited by 9 publications

(8 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“… 123 Another pathogenic pathway includes antigen-nonspecific T cell contact-mediated activation of macrophages and fibroblasts, acting through interactions between cluster of differentiation 40 (CD40) and CD40 ligands (CD40L), CD200 and CD200L, and intracellular adhesion molecule 1 and leucocyte function-associated antigen 1. 124 Ye et al 125 recently found that casein kinase II is an important regulator of the Th1 and Th17 cell axes and can aggravate the development of RA. 125 …”

Section: T Helper Cells Are Involved In the Immunomodulatory Process ...mentioning

confidence: 99%

See 1 more Smart Citation

Immunomodulatory role of T helper cells in rheumatoid arthritis

Luo

Wang

et al. 2022

Bone & Joint Research

View full text Add to dashboard Cite

Rheumatoid arthritis (RA) is an autoimmune disease that involves T and B cells and their reciprocal immune interactions with proinflammatory cytokines. T cells, an essential part of the immune system, play an important role in RA. T helper 1 (Th1) cells induce interferon-γ (IFN-γ), tumour necrosis factor-α (TNF-α), and interleukin (IL)-2, which are proinflammatory cytokines, leading to cartilage destruction and bone erosion. Th2 cells primarily secrete IL-4, IL-5, and IL-13, which exert anti-inflammatory and anti-osteoclastogenic effects in inflammatory arthritis models. IL-22 secreted by Th17 cells promotes the proliferation of synovial fibroblasts through induction of the chemokine C-C chemokine ligand 2 (CCL2). T follicular helper (Tfh) cells produce IL-21, which is key for B cell stimulation by the C-X-C chemokine receptor 5 (CXCR5) and coexpression with programmed cell death-1 (PD-1) and/or inducible T cell costimulator (ICOS). PD-1 inhibits T cell proliferation and cytokine production. In addition, there are many immunomodulatory agents that promote or inhibit the immunomodulatory role of T helper cells in RA to alleviate disease progression. These findings help to elucidate the aetiology and treatment of RA and point us toward the next steps. Cite this article: Bone Joint Res 2022;11(7):426–438.

show abstract

Section: T Helper Cells Are Involved In the Immunomodulatory Process ...mentioning

confidence: 99%

“… 124 Ye et al 125 recently found that casein kinase II is an important regulator of the Th1 and Th17 cell axes and can aggravate the development of RA. 125 …”

Section: T Helper Cells Are Involved In the Immunomodulatory Process ...mentioning

confidence: 99%

Immunomodulatory role of T helper cells in rheumatoid arthritis

Luo

Wang

et al. 2022

Bone & Joint Research

View full text Add to dashboard Cite

show abstract

“…Since RA is characterized by an imbalance of Tregs and Th17s, numerous studies have suggested that targeting Th cell subtypes could alleviate RA progression. Ye et al [ 37 ] utilized the CK2 inhibitor CX4945 to inhibit Th1 and Th17 cell responses while promoting Th2 cell responses in RA, which significantly dampened IFN- γ and IL-17A production and alleviated the inflammatory state. Rao et al [ 38 ] identified an expanded population of PD-1 hi CXCR5- “peripheral helper T (TPH) cells that express factors that enable the activation of B cells, including IL-21, CXCL13, ICOS, and MAF, with the application of multidimensional cytometry, transcriptomics, and functional assays”.…”

Section: Discussionmentioning

confidence: 99%

Identification and Verification of Novel Biomarkers Involving Rheumatoid Arthritis with Multimachine Learning Algorithms: An In Silicon and In Vivo Study

Liu,

Ye,

Wang

et al. 2024

Mediators of Inflammation

View full text Add to dashboard Cite

Background. Rheumatoid arthritis (RA) remains one of the most prevalent chronic joint diseases. However, due to the heterogeneity among RA patients, there are still no robust diagnostic and therapeutic biomarkers for the diagnosis and treatment of RA. Methods. We retrieved RA-related and pan-cancer information datasets from the Gene Expression Omnibus and The Cancer Genome Atlas databases, respectively. Six gene expression profiles and corresponding clinical information of GSE12021, GSE29746, GSE55235, GSE55457, GSE77298, and GSE89408 were adopted to perform differential expression gene analysis, enrichment, and immune component difference analyses of RA. Four machine learning algorithms, including LASSO, RF, XGBoost, and SVM, were used to identify RA-related biomarkers. Unsupervised cluster analysis was also used to decipher the heterogeneity of RA. A four-signature-based nomogram was constructed and verified to specifically diagnose RA and osteoarthritis (OA) from normal tissues. Consequently, RA-HFLS cell was utilized to investigate the biological role of CRTAM in RA. In addition, comparisons of diagnostic efficacy and biological roles among CRTAM and other classic biomarkers of RA were also performed. Results. Immune and stromal components were highly enriched in RA. Chemokine- and Th cell-related signatures were significantly activated in RA tissues. Four promising and novel biomarkers, including CRTAM, PTTG1IP, ITGB2, and MMP13, were identified and verified, which could be treated as novel treatment and diagnostic targets for RA. Nomograms based on the four signatures might aid in distinguishing and diagnosing RA, which reached a satisfactory performance in both training (AUC = 0.894) and testing (AUC = 0.843) cohorts. Two distinct subtypes of RA patients were identified, which further verified that these four signatures might be involved in the immune infiltration process. Furthermore, knockdown of CRTAM could significantly suppress the proliferation and invasion ability of RA cell line and thus could be treated as a novel therapeutic target. CRTAM owned a great diagnostic performance for RA than previous biomarkers including MMP3, S100A8, S100A9, IL6, COMP, LAG3, and ENTPD1. Mechanically, CRTAM could also be involved in the progression through immune dysfunction, fatty acid metabolism, and genomic instability across several cancer subtypes. Conclusion. CRTAM, PTTG1IP, ITGB2, and MMP13 were highly expressed in RA tissues and might function as pivotal diagnostic and treatment targets by deteriorating the immune dysfunction state. In addition, CRTAM might fuel cancer progression through immune signals, especially among RA patients.

show abstract

“…Single‐cell suspensions were prepared by isolating lymphocytes with mouse’ spleen lymphocyte isolation medium (TBD). Cells were resuspended in DMEM medium containing 10% FBS and 1% penicillin‐streptomycin, 5 × 10 5 cells per well were plated in 24‐well plates, and stimulated with PMA/Ionomycin Mixture (250X) (MULTI SCIENCES) of 4 μL for 12 h 23,24 . Then, 1 μL BFA (Biolegend) was added to each well to block the secretion of intracellular cytokines for 6 h 25,26 .…”

Section: Methodsmentioning

confidence: 99%

Tumor cell vaccine combined with Newcastle disease virus promote immunotherapy of lung cancer

Wang

Nan

Zhou

et al. 2023

Journal of Medical Virology

View full text Add to dashboard Cite

Lung cancer is a fatal disease with the highest worldwide morbidity and mortality rates. Despite recent advances in targeted therapy and immune checkpoint inhibitors for cancer, their efficacy remained limited. Therefore, we designed a Newcastle disease virus (NDV)‐modified tumor whole‐cell vaccine as a therapeutic vaccine and identified its antigen presentation level to develop effective immunotherapy. Then, we calculated the therapeutic and immune‐stimulating effects of NDV‐modified lung cancer cell vaccine and intratumoral NDV injection combination on tumor‐bearing mice. The results showed that the immunogenic cell death (ICD) expression in NDV‐modified lung cancer cell vaccine stimulates dendritic cell maturation and T cell activation in vivo and in vitro. Moreover, NDV‐modified lung cancer cell vaccine combined with intratumoral NDV injection could significantly inhibit tumor growth and enhance the differentiation of Th1 cells and Inflammatory cell infiltration in vivo, leading to an excellent immunotherapeutic effect. Therefore, our results revealed that NDV‐modified lung cancer cell vaccine combined with intratumoral NDV injection could promote antigen presentation and induce a strong antitumor immune response, which provided a promising combined therapy strategy for tumor immunotherapy.

show abstract

Casein Kinase II exacerbates rheumatoid arthritis via promoting Th1 and Th17 cell inflammatory responses

Cited by 9 publications

References 26 publications

Immunomodulatory role of T helper cells in rheumatoid arthritis

Immunomodulatory role of T helper cells in rheumatoid arthritis

Identification and Verification of Novel Biomarkers Involving Rheumatoid Arthritis with Multimachine Learning Algorithms: An In Silicon and In Vivo Study

Tumor cell vaccine combined with Newcastle disease virus promote immunotherapy of lung cancer

Contact Info

Product

Resources

About