Dear Colleagues,
The immune response system in rheumatoid arthritis involves a complex combination of innate and acquired immunity that frequently elicits inflammatory responses to pathogens resulting in infections and internal danger signals that can eliminate harmful factors. Cytokines are small secreted proteins involved in immune homeostasis, but they are also involved in the pathogenesis of several autoimmune and inflammatory diseases. Signaling from cytokine receptors bound to cell membranes is a complex network that leads to gene expression and ultimately regulates cellular function. Our understanding of the intracellular actions of interleukins such as interferon, and tumor necrosis factor has been greatly advanced in the past few years, making it possible to interfere with the cytokine signaling cascade. The Janus kinase/transcriptional signaling activator, nuclear factor kappa-light chain-activated B cell enhancer, mitogen-activated protein kinase, and phosphatidylinositol 3'-kinase pathways have been intensively studied and key steps and molecules identified. These research efforts have led to the development of a new generation of small molecule inhibitors. Thus, the challenge to elucidate the pathogenesis of rheumatoid arthritis requires expert analysis of the molecular and cellular basis of the disease and clinical studies.
This research topic aims to discuss the cytokine network from a pathogenetic perspective. It will be important to select cytokine targets not from a single inflammatory pathway, but from a pathological biosystem approach. We expect a lively exchange of views through this special issue, not only on basic research on biologics and Janus kinase inhibitors, but also on clinical research, which will be widely accepted.
Assoc. Prof. Yuji Nozaki
Guest Editor
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