About this Research Topic
This Research Topic is the second volume of the “Th2-Associated Immunity in The Pathogenesis of Systemic Lupus Erythematosus and Rheumatoid Arthritis” Community Series. Please see Volume I here
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.
The Topic Editors declare no competing interests with regard to the Research Topic subject.
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.
The Topic Editors declare no competing interests with regard to the Research Topic subject.
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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