Absence of signaling into CD4 + cells via C3aR and C5aR enables autoinductive TGF-β1 signaling and induction of Foxp3 + regulatory T cells
TLDR
The absence of signaling via C3aR and C5aR resulted in lower expression of costimulatory molecules and interleukin 6 (IL-6) and more production of IL-10, which suppressed ongoing autoimmune disease.Abstract:
Complement provides costimulatory signals to T cells. Medof and colleagues demonstrate that an absence of complement signaling in naive T cells generates an autoinductive loop to drive induced regulatory T cells.read more
Citations
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Transforming Growth Factor-β Signaling in Immunity and Cancer.
Eduard Batlle,Joan Massagué +1 more
TL;DR: An overview of the complex biology of the TGF-β family and its context-dependent nature is presented and how this knowledge is being leveraged to unleash the immune system against the tumor is discussed.
Journal ArticleDOI
Keeping It All Going—Complement Meets Metabolism
Martin Kolev,Claudia Kemper +1 more
TL;DR: Current knowledge about complement’s emerging relationship with the cellular metabolism machinery is covered with a focus on the functional differences between serum-circulating versus intracellularly active complement during normal cell survival and induction of effector functions.
Journal ArticleDOI
Complement System Part II: Role in Immunity.
Nicolas S. Merle,Remi Noe,Lise Halbwachs-Mecarelli,Véronique Frémeaux-Bacchi,Lubka T. Roumenina +4 more
TL;DR: Recent advances in the understanding of the role of complement in physiology and pathology are discussed, showing that complement contributes to a large variety of conditions, far exceeding the classical examples of diseases associated with complement deficiencies.
Journal ArticleDOI
Development and Maintenance of Regulatory T cells
TL;DR: Understanding how epigenetic alterations and Foxp3 expression coordinately control Treg-cell-specific gene regulation will enable better control of immune responses by targeting the generation and maintenance of Treg cells.
Journal ArticleDOI
Overview of complement activation and regulation.
Marina Noris,Giuseppe Remuzzi +1 more
TL;DR: Many kidney disorders have been linked to abnormal complement activation, including immune-complex–mediated glomerulonephritis and rare genetic kidney diseases, but also tubulointerstitial injury associated with progressive proteinuric diseases or ischemia-reperfusion.
References
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Journal ArticleDOI
Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells.
Estelle Bettelli,Yijun Carrier,Wenda Gao,Thomas Korn,Terry B. Strom,Mohamed Oukka,Howard L. Weiner,Vijay K. Kuchroo +7 more
TL;DR: It is shown that IL-6, an acute phase protein induced during inflammation, completely inhibits the generation of Foxp3+ Treg cells induced by TGF-β, and the data demonstrate a dichotomy in thegeneration of pathogenic (TH17) T cells that induce autoimmunity and regulatory (Foxp3+) T Cells that inhibit autoimmune tissue injury.
Journal ArticleDOI
Mechanisms of foxp3+ T regulatory cell-mediated suppression.
TL;DR: The in vitro model systems that have been developed to define the mechanisms used by Treg cells to suppress a large number of distinct target cell types are reviewed.
Journal ArticleDOI
Regulatory T cells exert checks and balances on self tolerance and autoimmunity
TL;DR: New ways of treating immunological diseases by targeting Treg cells at the cellular and molecular levels are envisaged.
Journal ArticleDOI
Transient expression of FOXP3 in human activated nonregulatory CD4+ T cells.
TL;DR: Exposure of endogenous FOXP3, in humans, is not sufficient to induce regulatory T cell activity or to identify Treg cells, as it is demonstrated that it is also expressed in activated nonsuppressive T cells.
Journal ArticleDOI
How are T H 2-type immune responses initiated and amplified?
William E. Paul,Jinfang Zhu +1 more
TL;DR: The involvement of allergen- and parasite product-mediated activation of epithelial cells, basophils and dendritic cells and the functions of the cytokines interleukin-4 (IL-4), IL-25, IL-33 and thymic stromal lymphopoietin in the initiation and amplification of TH2-type immune responses in vivo are discussed.
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