T follicular helper cell subsets: a potential key player in autoimmunity

Kurata, Izumi; Matsumoto, Isao; Sumida, Takayuki

doi:10.1080/25785826.2020.1776079

Cited by 48 publications

(43 citation statements)

References 95 publications

(143 reference statements)

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“…These fates determine the roles of terminal Tfh cells in the immune response. The Tfh1 differentiation pathway can be initiated by type 1 responses in which STAT1/4-activating cytokines expand, such as viral infection, vaccination, or some autoimmune diseases ( 9 , 10 , 12 , 13 ). Tfh1-source subsets produce IFN-γ and IL-21 and lead to isotype switching of GC B cells to induce murine IgG 2 or human IgG 1 ( 14 ).…”

Section: Functional Diversity Of Tfh Cellsmentioning

confidence: 99%

Multi-Source Pathways of T Follicular Helper Cell Differentiation

Nakayamada

2021

Front. Immunol.

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T follicular helper (Tfh) cells participate in humoral immune by promoting inflammation and aiding B cells survival, proliferation, maturation, and generation autoantibodies. The plasticity of Tfh cells enables the immune system to adjust the direction of differentiation according to the degree of the immune response, regulate the germinal center (GC) response and maintain homeostasis. Tfh differentiation involves several signaling factors, including multiple cytokines, receptors, transcription factors and genes. The signal transducer and activator of transcription (STAT) family signaling pathways are crucial for Tfh formation. However, because of the multi-factorial and multi-stage features of Tfh differentiation, every STAT member plays a role in Tfh differentiation, but is not completely depended on. With the gradual recognition of different Tfh subsets (Tfh1, Tfh2, Tfh17), the process of Tfh differentiation can no longer be explained by straight-line derivation models. In this review, we summarize the roles of different STATs in mediating Tfh subsets, analyze the contributions of mutual restraint and cooperation among cytokine-STAT signals to terminal Tfh differentiation, and clarify the multi-source pathways of Tfh differentiation with a three-dimensional illustration.

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Section: Functional Diversity Of Tfh Cellsmentioning

confidence: 99%

Multi-Source Pathways of T Follicular Helper Cell Differentiation

Nakayamada

2021

Front. Immunol.

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“…And even if Tfh cells are needed—will they develop from naïve T cells, or could other T‐helper lineages develop into Tfh cells in MALT? Different types of Tfh cells that share phenotype with other lineages have been described, making them Tfh1, Tfh2, or Tfh17 cells; do these develop when Tfh cells differentiated toward other phenotypes or do Th1, Th2, and Th17 cells become Tfh cells 173,174 . And what about T follicular regulatory (Tfr) cells—they seem to develop primarily from thymic T regulatory cells but can they also be derived from induced regulatory T cells or even naïve cells 175 …”

Section: T Cells Contributing To Iga Responsesmentioning

confidence: 99%

Know your enemy or find your friend?—Induction of IgA at mucosal surfaces

Bemark

Angeletti

2021

Immunological Reviews

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Most antibodies produced in the body are of the IgA class. The dominant cell population producing them are plasma cells within the lamina propria of the gastrointestinal tract, but many IgA‐producing cells are also found in the airways, within mammary tissues, the urogenital tract and inside the bone marrow. Most IgA antibodies are transported into the lumen by epithelial cells as part of the mucosal secretions, but they are also present in serum and other body fluids. A large part of the commensal microbiota in the gut is covered with IgA antibodies, and it has been demonstrated that this plays a role in maintaining a healthy balance between the host and the bacteria. However, IgA antibodies also play important roles in neutralizing pathogens in the gastrointestinal tract and the upper airways. The distinction between the two roles of IgA ‐ protective and balance‐maintaining ‐ not only has implications on function but also on how the production is regulated. Here, we discuss these issues with a special focus on gut and airways.

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“…This will ultimately lead to immunoglobulin isotype switching and the production of long-lasting plasma cells. It has been shown that the frequency of Tfh cells is correlated with lymphocytic infiltration, the number of B cells, elevated serum and salivary gland Ig levels, and autoimmunity [ 68 , 69 ]. Tfh cells can also be found in the peripheral circulation and can be identified by CXCR5 expression on CD4 T-cells with flow cytometry [ 13 ].…”

Section: Immune Monitoring—the “How”mentioning

confidence: 99%

Immune Monitoring upon Treatment with Biologics in Sjögren’s Syndrome: The What, Where, When, and How

Beers

Damoiseaux

2021

Biomolecules

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Over the years, a wide variety of therapeutic antibodies has been successfully introduced in the auto-immunology clinic, and many more are on the way. Many of these treatments address either a pathogenic circulating molecule or a cell-bound molecule. Whereas addressing the former target results in neutralization of the soluble factor and binding to the latter target either inhibits cellular function or induces selective cell death. If this targeted molecule or cell is part of the immune system, this therapy evokes a state of immunodeficiency with infections as a possible consequence. Therefore, immune monitoring is needed to prevent such adverse side effects of immunotherapy. In this paper, different immunotherapies used in Sjögren’s syndrome, as well as different approaches to monitoring the immune system, are discussed.

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T follicular helper cell subsets: a potential key player in autoimmunity

Cited by 48 publications

References 95 publications

Multi-Source Pathways of T Follicular Helper Cell Differentiation

Multi-Source Pathways of T Follicular Helper Cell Differentiation

Know your enemy or find your friend?—Induction of IgA at mucosal surfaces

Immune Monitoring upon Treatment with Biologics in Sjögren’s Syndrome: The What, Where, When, and How

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