About this Research Topic
In recent years, increasing evidence has shown that Th2-associated immunity plays a key role in autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA), and is expected to contribute to disease diagnosis and prognosis (e.g. biomarker), and targeted therapy.
T helper (Th) cells can provide helper functions to other immune cells (macrophages, dendritic cells, B cells, etc.) for their activation and maturation. Th subsets are characterized by the cytokines they secrete and effector functions they perform. Th2 cells mediate the activation and maintenance of humoral, or antibody-mediated immune response by producing various cytokines (IL-4, IL-5, IL-6, IL-9, IL-10, IL-13, and IL-25, etc), extracellular vesicles (EVs), and/or directly contact with target cells. In addition, Th2-associated immunity also includes other factors, such as basophils, mast cells, IgE, IgG4, Th2-related transcriptional factors (Pparγ, Gata3, etc.) and pathways (JAK-STAT signaling, Batf/Irf4, Bach2/Batf pathway, etc.). However, detailed molecular regulation mechanisms of Th2-associated immunity in the pathogenesis of SLE and RA still need to be further investigated. Understanding the mechanism of Th2-associated immunity in the pathogenesis of SLE and RA its future clinical application needs more discussion and verification.
The goal of this Research Topic is to provide a forum for advanced research on the contribution of Th2-associated immunity to the pathogenesis and prevention of SLE and RA as well as to explore innovative Th2-associated immunity-oriented pharmacological interventions in the attempt to achieve a beneficial impact on SLE and RA.
We welcome submissions of Original Research and Review articles on the following aspects:
- Role and mechanisms of Th2 cells in the activation and maintenance of the humoral, or antibody-mediated, immune response, and how it contributes to the pathogenesis and prevention of SLE and RA;
- Role and mechanisms of extracellular vesicles (EVs), cytokines (IL-4, IL-5, IL-6, IL-9, IL-10, IL-13, and IL-25, etc), and/or directly contact in the interaction of Th2 cells and target cells (macrophages, dendritic cells, B cells, Treg, Breg, etc.), and how they play roles in the pathogenesis and prevention of SLE and RA;
- Role and mechanisms of Th2-associated immunity, such as basophils, mast cells, IgE, IgG4, Th2-related transcriptional factors (Pparγ, Gata3, etc.) and pathways (JAK-STAT signaling, Batf/Irf4, Bach2/Batf pathway, etc.), in the pathogenesis and prevention of SLE and RA.
T helper (Th) cells can provide helper functions to other immune cells (macrophages, dendritic cells, B cells, etc.) for their activation and maturation. Th subsets are characterized by the cytokines they secrete and effector functions they perform. Th2 cells mediate the activation and maintenance of humoral, or antibody-mediated immune response by producing various cytokines (IL-4, IL-5, IL-6, IL-9, IL-10, IL-13, and IL-25, etc), extracellular vesicles (EVs), and/or directly contact with target cells. In addition, Th2-associated immunity also includes other factors, such as basophils, mast cells, IgE, IgG4, Th2-related transcriptional factors (Pparγ, Gata3, etc.) and pathways (JAK-STAT signaling, Batf/Irf4, Bach2/Batf pathway, etc.). However, detailed molecular regulation mechanisms of Th2-associated immunity in the pathogenesis of SLE and RA still need to be further investigated. Understanding the mechanism of Th2-associated immunity in the pathogenesis of SLE and RA its future clinical application needs more discussion and verification.
The goal of this Research Topic is to provide a forum for advanced research on the contribution of Th2-associated immunity to the pathogenesis and prevention of SLE and RA as well as to explore innovative Th2-associated immunity-oriented pharmacological interventions in the attempt to achieve a beneficial impact on SLE and RA.
We welcome submissions of Original Research and Review articles on the following aspects:
- Role and mechanisms of Th2 cells in the activation and maintenance of the humoral, or antibody-mediated, immune response, and how it contributes to the pathogenesis and prevention of SLE and RA;
- Role and mechanisms of extracellular vesicles (EVs), cytokines (IL-4, IL-5, IL-6, IL-9, IL-10, IL-13, and IL-25, etc), and/or directly contact in the interaction of Th2 cells and target cells (macrophages, dendritic cells, B cells, Treg, Breg, etc.), and how they play roles in the pathogenesis and prevention of SLE and RA;
- Role and mechanisms of Th2-associated immunity, such as basophils, mast cells, IgE, IgG4, Th2-related transcriptional factors (Pparγ, Gata3, etc.) and pathways (JAK-STAT signaling, Batf/Irf4, Bach2/Batf pathway, etc.), in the pathogenesis and prevention of SLE and RA.
Keywords: Th2, Th2-associated immunity, Pathogenesis, IgG4, IgE, Basophil, Mast cell, Il-4, Il-13, Autoimmunity, B cell, T cell, Inflammation, Systemic lupus erythematosus, Rheumatoid arthritis
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