Rheumatoid arthritis (RA) is a progressive autoimmune disease mainly characterized by synovitis and joint damage, often leading to polyarthritis. As a common autoimmune disease, the global incidence rate of RA is approximately 0.5-1.0%. Several autoantibodies, such as anti-citrullinated protein antibodies (ACPA), and rheumatoid factor, are involved in the pathogenesis of RA. The association of the disease with HLA-DRB1 alleles that share a 70-74 amino acid(aa) sequence (HLA-DRB1 shared epitope) are indicative of the autoimmune nature of RA. B cells play crucial roles in autoantibody secretion and control the development of RA. ACPAs play a pathogenic role in RA via immune complexes, neutrophil extracellular trap (NET) formation, macrophage activation, synovial fibroblast adhesion and migration, and osteoclast activation. This leads to the destruction of joint tissues. There is a suggestion that environmental agents, via molecular mimicry, activate T cells, which in turn activate B cells initiating the typical inflammatory cascade in RA, with the production of proinflammatory cytokines, resulting in the joint damage often seen. Monoclonal antibodies directed against these proinflammatory agents mediators, and small oral molecules directed against proinflammatory cytokines have been used effectively in the treatment of RA.
Although conventional and immunosuppressive therapies are effective in the treatment of RA, the existence of side effects greatly limits the long-term disease outcomes. Epigenetics can regulate gene expression and the study of this has received much attention in recent years, particularly microRNAs(miRNAs). Various miRNAs were abnormal in RA and could be used as biomarkers for disease diagnosis, disease activity and disease manifestations The first RNA interference drug, developed in 2018 marked the beginning of a new era for the treatment of hereditary transthyretin-mediated amyloidosis. RNA-based strategies may directly interfere with key inflammatory signaling pathways in RA patients and shed a light on the treatment of RA.
Certain autoantibodies can be detected during the progression of RA and previous studies have reported the effects of autoantibodies in RA patients. Further serological profiling of autoantibody maps in RA patients and the mechanistic study of novel autoantibodies, B cell subsets and B cell function during disease progression and joint damages in RA patients and mouse models may provide new therapeutic targets in RA treatment. Further, recent studies show that lipid-based nanoparticles (LNP) have been significantly advanced and may promote the development of a more effective LNP-based siRNA delivery system. Pharmacoepigenetics is also an emerging field in medicine and miRNAs could be enhanced or neutralized therapeutically to inhibit inflammation in RA and other autoimmune disorders.
Therefore, the mechanistic study of B cell function, autoantibody effects and invention of RNA drug delivery systems will be explored in this article collection.
This Research Topic welcomes submissions related to autoantibodies and RNA therapy in RA, with manuscripts focusing on, but not limited to, the following specific topics:
• Novel therapeutic strategy for RA using microRNA
• RNA regulation of Th cell response in Patients with RA
• B cell associated cytokine regulation in RA
• Antibodies promoting pathogenic bone resorption in RA
• B cells involved in pathogenic mechanisms and treatment of RA
• Novel treatment methods utilizing Lipid based nanoparticles
• miRNA as biomarkers
Rheumatoid arthritis (RA) is a progressive autoimmune disease mainly characterized by synovitis and joint damage, often leading to polyarthritis. As a common autoimmune disease, the global incidence rate of RA is approximately 0.5-1.0%. Several autoantibodies, such as anti-citrullinated protein antibodies (ACPA), and rheumatoid factor, are involved in the pathogenesis of RA. The association of the disease with HLA-DRB1 alleles that share a 70-74 amino acid(aa) sequence (HLA-DRB1 shared epitope) are indicative of the autoimmune nature of RA. B cells play crucial roles in autoantibody secretion and control the development of RA. ACPAs play a pathogenic role in RA via immune complexes, neutrophil extracellular trap (NET) formation, macrophage activation, synovial fibroblast adhesion and migration, and osteoclast activation. This leads to the destruction of joint tissues. There is a suggestion that environmental agents, via molecular mimicry, activate T cells, which in turn activate B cells initiating the typical inflammatory cascade in RA, with the production of proinflammatory cytokines, resulting in the joint damage often seen. Monoclonal antibodies directed against these proinflammatory agents mediators, and small oral molecules directed against proinflammatory cytokines have been used effectively in the treatment of RA.
Although conventional and immunosuppressive therapies are effective in the treatment of RA, the existence of side effects greatly limits the long-term disease outcomes. Epigenetics can regulate gene expression and the study of this has received much attention in recent years, particularly microRNAs(miRNAs). Various miRNAs were abnormal in RA and could be used as biomarkers for disease diagnosis, disease activity and disease manifestations The first RNA interference drug, developed in 2018 marked the beginning of a new era for the treatment of hereditary transthyretin-mediated amyloidosis. RNA-based strategies may directly interfere with key inflammatory signaling pathways in RA patients and shed a light on the treatment of RA.
Certain autoantibodies can be detected during the progression of RA and previous studies have reported the effects of autoantibodies in RA patients. Further serological profiling of autoantibody maps in RA patients and the mechanistic study of novel autoantibodies, B cell subsets and B cell function during disease progression and joint damages in RA patients and mouse models may provide new therapeutic targets in RA treatment. Further, recent studies show that lipid-based nanoparticles (LNP) have been significantly advanced and may promote the development of a more effective LNP-based siRNA delivery system. Pharmacoepigenetics is also an emerging field in medicine and miRNAs could be enhanced or neutralized therapeutically to inhibit inflammation in RA and other autoimmune disorders.
Therefore, the mechanistic study of B cell function, autoantibody effects and invention of RNA drug delivery systems will be explored in this article collection.
This Research Topic welcomes submissions related to autoantibodies and RNA therapy in RA, with manuscripts focusing on, but not limited to, the following specific topics:
• Novel therapeutic strategy for RA using microRNA
• RNA regulation of Th cell response in Patients with RA
• B cell associated cytokine regulation in RA
• Antibodies promoting pathogenic bone resorption in RA
• B cells involved in pathogenic mechanisms and treatment of RA
• Novel treatment methods utilizing Lipid based nanoparticles
• miRNA as biomarkers
