About this Research Topic
The Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway plays pivotal roles in the regulation of immune system, especially in transduction of cytokine signaling. This pathway can counterbalance the polarization of T cells. Four types of JAKs (JAK1-3 and Tyk2) are responsible for signal transduction through type 1 and type 2 cytokine receptors. After binding of cytokine ligands to their specific receptors, JAKs transphosphorylate each other and subsequently seven types of STATS. Homodimerized or heterodimerized STATS translocate to the nucleus either to activate or inhibit gene expression. The JAK-STAT pathway is regulated by several regulator proteins, including Suppressors of Cytokine Signaling (SOCS), Protein Inhibitors of Activated STATs (PIAS) and Protein Tyrosine Phosphatases (PTPs), delineating the initiation, duration and termination of the signaling cascades and consequently the fate of T cells. Dysregulation of the JAK-STAT pathway in T helper cells may result in various immune-related disorders such as allergic and autoimmune disease.
Modulation of the JAK-STAT pathway may deviate T cells toward Th1/Th17 cells or Th2 cells that are involved in inflammatory and anti-inflammatory conditions, respectively. In particular, Th1/Th17 cells are prominent cells in autoimmune diseases, while Th2 cells are dominant cells in allergic diseases. STAT1 and STAT4 are activated in Th1 cells by Interferon gamma and Interleukin-12 (IL-12), respectively. On the other hand, STAT6 is activated in Th2 cells by IL-4. Finally, STAT3 is activated in Th17 cells by IL-6. Accordingly, T cell polarization may be affected by alteration of JAK-STAT signaling to manage homeostasis and counterbalance Th1/Th17 and Th2 arms of immune system.
This research topic aims to provide an overview to spread principal knowledge underlying cellular and molecular mechanisms on JAK-STAT signaling for counterbalancing of T cell polarization in allergic and autoimmune diseases. Novel promising therapies regarding the targeting of JAK-STAT pathway by JAK inhibitors (JAKinibs), antagonistic-agonistic antibodies, secretory-excretory products used in helminth therapy, herbal medicine, and other therapeutic agents are appreciated. Original research papers that contain novel and prominent information of general interest to researchers in these fields are highly appreciated. Adequate details must be prepared to enable other researchers to reproduce the study. In addition, reviews and mini reviews are welcome. Particularly welcome are papers dealing with:
• Regulation/dysregulation of JAK-STAT signaling in allergic and autoimmune diseases.
•JAK-STAT信号调制(JAKinibs)for T cell polarization.
• Cytokine receptor blockade (antagonists and agonists) by monoclonal antibodies or new therapeutic agents for counterbalancing Th cell polarization.
• Novel microRNA biomarkers for assessment of JAKinib efficacy in allergic and autoimmune diseases.
When you submit your paper through Frontiers in Immunology Editorial Manager, please identify your contribution to be part of this Special Issue.
Topic Editor Dr. Meylan is employed by Innovent Biologics. The other Topic Editors declare no competing interests with regard to the Research Topic subject.
Modulation of the JAK-STAT pathway may deviate T cells toward Th1/Th17 cells or Th2 cells that are involved in inflammatory and anti-inflammatory conditions, respectively. In particular, Th1/Th17 cells are prominent cells in autoimmune diseases, while Th2 cells are dominant cells in allergic diseases. STAT1 and STAT4 are activated in Th1 cells by Interferon gamma and Interleukin-12 (IL-12), respectively. On the other hand, STAT6 is activated in Th2 cells by IL-4. Finally, STAT3 is activated in Th17 cells by IL-6. Accordingly, T cell polarization may be affected by alteration of JAK-STAT signaling to manage homeostasis and counterbalance Th1/Th17 and Th2 arms of immune system.
This research topic aims to provide an overview to spread principal knowledge underlying cellular and molecular mechanisms on JAK-STAT signaling for counterbalancing of T cell polarization in allergic and autoimmune diseases. Novel promising therapies regarding the targeting of JAK-STAT pathway by JAK inhibitors (JAKinibs), antagonistic-agonistic antibodies, secretory-excretory products used in helminth therapy, herbal medicine, and other therapeutic agents are appreciated. Original research papers that contain novel and prominent information of general interest to researchers in these fields are highly appreciated. Adequate details must be prepared to enable other researchers to reproduce the study. In addition, reviews and mini reviews are welcome. Particularly welcome are papers dealing with:
• Regulation/dysregulation of JAK-STAT signaling in allergic and autoimmune diseases.
•JAK-STAT信号调制(JAKinibs)for T cell polarization.
• Cytokine receptor blockade (antagonists and agonists) by monoclonal antibodies or new therapeutic agents for counterbalancing Th cell polarization.
• Novel microRNA biomarkers for assessment of JAKinib efficacy in allergic and autoimmune diseases.
When you submit your paper through Frontiers in Immunology Editorial Manager, please identify your contribution to be part of this Special Issue.
Topic Editor Dr. Meylan is employed by Innovent Biologics. The other Topic Editors declare no competing interests with regard to the Research Topic subject.
Keywords: JAK-STAT signaling, T cell, allergic and autoimmune diseases, cytokine receptor, SOCS, PIAS, PTP, monoclonal antibody, Th1, Th2, Th17, herbal medicine, microRNA
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
