Foxp3-Mediated Suppression of CD95L Expression Confers Resistance to Activation-Induced Cell Death in Regulatory T Cells

Weiß, Eva-Maria; Schmidt, Angelika; Vobis, Diana; Garbi, Natalio; Lahl, Katharina; Mayer, Christian T.; Sparwasser, Tim; Ludwig, Andreas; Suri‐Payer, Elisabeth; Oberle, Nina; Krammer, Peter H.

doi:10.4049/jimmunol.1002321

Cited by 50 publications

(55 citation statements)

References 43 publications

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“…The most significantly different markers were CD95, CCR4, and CD45RO. [36][37][38] The identified Treg subpopulations were compared with established Treg subpopulation definitions. 23 Although Tregs A and B overlap with Treg subpopulations I and II, respectively, our approach demarcates those Treg III cells that are closer to Tregs and combine them with subpopulation A or B based on their phenotype and eliminate cells that are closer to T con and less likely to be regulatory.…”

Section: Discussionmentioning

confidence: 99%

Deep phenotyping of Tregs identifies an immune signature for idiopathic aplastic anemia and predicts response to treatment

Kordasti

Costantini

Seidl

et al. 2016

Blood

121

115

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Key Points• hi , CD127 lo Tregs), expresses the interleukin-2 (IL-2)/STAT5 pathway and cell-cycle commitment genes. Furthermore, in vitro-expanded Tregs become functional and take on the characteristics of Treg B. Collectively, this study identifies human Treg subpopulations that can be used as predictive biomarkers for response to IST in AA and potentially other autoimmune diseases. We also show that Tregs from AA patients are IL-2-sensitive and expandable in vitro, suggesting novel therapeutic approaches such as low-dose IL-2 therapy and/or expanded autologous Tregs and meriting further exploration. (Blood. 2016;128(9):1193-1205

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Section: Discussionmentioning

confidence: 99%

Deep phenotyping of Tregs identifies an immune signature for idiopathic aplastic anemia and predicts response to treatment

Kordasti

Costantini

Seidl

et al. 2016

Blood

121

115

View full text Add to dashboard Cite

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“…Fas/FasL also induced apoptosis in Tregs (128). The Fas/FasL pathway alone cannot induce immune tolerance (129).…”

Section: T Effectors Die Of Activation-induced Cell Deathmentioning

confidence: 99%

T Cells

Hall

2015

Clinical Journal of the American Society of Nephrology

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Traditionally, T cells were CD4 1 helper or CD8 1 cytotoxic T cells, and with antibodies, they were the soldiers of immunity. Now, many functionally distinct subsets of activated CD4 1 and CD8 1 T cells have been described, each with distinct cytokine and transcription factor expression. For CD4 1 T cells, these include Th1 cells expressing the transcription factor T-bet and cytokines IL-2, IFN-g, and TNF-b; Th2 cells expressing GATA-3 and the cytokines IL-4, IL-5, and IL-13; and Th17 cells expressing RORgt and cytokines IL-17A, IL-17F, IL-21, and IL-22. The cytokines produced determine the immune inflammation that they mediate. T cells of the effector lineage can be naïve T cells, recently activated T cells, or memory T cells that can be distinguished by cell surface markers. T regulatory cells or spies were characterized as CD8 1 T cells expressing I-J in the 1970s. In the 1980s, suppressor cells fell into disrepute when the gene for I-J was not present in the mouse MHC I region. At that time, a CD4 1 T cell expressing CD25, the IL-2 receptor-a, was identified to transfer transplant tolerance. This was the same phenotype of activated CD4 1 CD25 1 T cells that mediated rejection. Thus, the cells that could induce tolerance and undermine rejection had similar badges and uniforms as the cells effecting rejection. Later, FOXP3, a transcription factor that confers suppressor function, was described and distinguishes T regulatory cells from effector T cells. Many subtypes of T regulatory cells can be characterized by different expressions of cytokines and receptors for cytokines or chemokines. In intense immune inflammation, T regulatory cells express cytokines characteristic of effector cells; for example, Th1-like T regulatory cells express T-bet, and IFN-g-like Th1 cells and effector T cells can change sides by converting to T regulatory cells. Effector T cells and T regulatory cells use similar molecules to be activated and mediate their function, and thus, it can be very difficult to distinguish soldiers from spies.

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“…Next, to further characterize the Treg-of-B1a cells, we used a number of molecules reported to be associated with the functions of Treg cells. [22][23][24][25][26][27][28][29][30] We found that Treg-of-B1a cells expressed a series of surface molecules, including ICOS, PD-1, GITR, OX40, IL-10R and TNFR2 (Figure 3b). Among them, ICOS, GITR, IL-10R and PD-1 were expressed at higher levels Therefore, B-1a cells are the major IL-10-producing cell population present in the steady-state peritoneal cavity, and they spontaneously produce IL-10 without any stimulation.…”

Section: B-1a Cells Convert Naive Cd4 1 T Cells Into Foxp3 2 Treg Cellsmentioning

confidence: 99%

A B-1a cell subset induces Foxp3− T cells with regulatory activity through an IL-10-independent pathway

Hsu

Chu

et al. 2014

Cell Mol Immunol

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Foxp3-Mediated Suppression of CD95L Expression Confers Resistance to Activation-Induced Cell Death in Regulatory T Cells

Cited by 50 publications

References 43 publications

Deep phenotyping of Tregs identifies an immune signature for idiopathic aplastic anemia and predicts response to treatment

Deep phenotyping of Tregs identifies an immune signature for idiopathic aplastic anemia and predicts response to treatment

T Cells

A B-1a cell subset induces Foxp3− T cells with regulatory activity through an IL-10-independent pathway

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