Research Topic

Th2-Associated Immunity in The Pathogenesis of Systemic Lupus Erythematosus and Rheumatoid Arthritis

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.


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


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.

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.


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


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.

About Frontiers Research Topics

With their unique mixes of varied contributions from Original Research to Review Articles, Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author.

Topic Editors

Loading..

Submission Deadlines

31 May 2021 Abstract
30 November 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

Loading..

Topic Editors

Loading..

Submission Deadlines

31 May 2021 Abstract
30 November 2021 Manuscript

Participating Journals

Manuscripts can be submitted to this Research Topic via the following journals:

Loading..
Loading..

total views article views article downloads topic views

}
 
Top countries
Top referring sites
Loading..