Induced CD4+ forkhead box protein–positive T cells inhibit mast cell function and established contact hypersensitivity through TGF-β1

Su, Wenru; Fan, Huimin; Chen, Maogen; Wang, Julie; Brand, David; He, Xiaoshun; Quesniaux, Valérie; Ryffel, Bernhard; Zhu, Ling; Liang, Dan; Zheng, Song Guo

doi:10.1016/j.jaci.2012.05.011

Cited by 53 publications

(39 citation statements)

References 59 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This system uses a semipermeable membrane (0.4 mm pore) that prevents cell-to-cell contact yet allows for the exchange of soluble mediators. This designed, which allows for an assessment of the impact of soluble mediators, has previously been described by Su and colleagues, who investigated the effect of T-regulatory cells on the function of mast cells (33), and by Wang and colleagues, who examined the inhibition of T-cell proliferation by mediators released by lung epithelial cells (32). The release of Ang-2 from PVEC monolayers indicates that only through direct EC/neutrophil interaction was Ang-2 significantly increased in assay supernatant.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Neutrophil–Endothelial Interactions Mediate Angiopoietin-2–Associated Pulmonary Endothelial Cell Dysfunction in Indirect Acute Lung Injury in Mice

Lomas-Neira

Venet

Chung

et al. 2014

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

Unresolved inflammation in the lung is thought to elicit loss of endothelial cell (EC) barrier integrity and impaired lung function. We have shown, in a mouse model of shock/sepsis, that neutrophil interactions with resident pulmonary cells appear central to the pathogenesis of indirect acute lung injury (iALI). Normally, EC growth factors angiopoietin (Ang)-1 and Ang-2 maintain vascular homeostasis through tightly regulated interaction with the kinase receptor Tie2 expressed on ECs. Although Ang-1/Tie2 has been shown to promote vessel integrity, stimulating downstream prosurvival/antiinflammatory signaling, Ang-2, released from activated ECs, is reported to promote vessel destabilization. This mechanism of regulation, together with recent clinical findings that plasma Ang-2 levels are significantly elevated in patients who develop acute respiratory distress syndrome, has focused our investigation on the contribution of Ang-2 to the development of iALI. A murine model of hemorrhagic shock-induced priming for the development of iALI after subsequent septic challenge was used in this study. Our findings show that 1) Ang-2 is elevated in our experimental model for iALI, 2) direct EC/neutrophil interactions contribute significantly to EC Ang-2 release, and 3) suppression of Ang-2 significantly decreases inflammatory lung injury, neutrophil influx, and lung and plasma IL-6 and TNF-α. These findings support our hypothesis and suggest that Ang-2 plays a role in the loss of pulmonary EC barrier function in the development of iALI in mice resultant from the sequential insults of hemorrhagic shock and sepsis and that this is mediated by EC interaction with activated neutrophils.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Ang-2 protein was measured in the supernatant. Other laboratories have previously published examples of this methodology (31)(32)(33).…”

Section: Model Of Ialimentioning

confidence: 99%

Neutrophil–Endothelial Interactions Mediate Angiopoietin-2–Associated Pulmonary Endothelial Cell Dysfunction in Indirect Acute Lung Injury in Mice

Lomas-Neira

Venet

Chung

et al. 2014

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

show abstract

“…IgE-mediated activation of MCs was performed as described in our previous study (8). In brief, MCs A β-hexosaminidase substrate assay was used to quantitate MC degranulation.…”

Section: 3ige-mediated Activation Of Mcsmentioning

confidence: 99%

Doxycycline exerts multiple anti-allergy effects to attenuate murine allergic conjunctivitis and systemic anaphylaxis

Wan

Han

et al. 2014

Biochemical Pharmacology

Self Cite

View full text Add to dashboard Cite

“…iTregs induced with IL-2 and TGF-β have proved to have a protective efficacy in many kinds of disease models, including collagen induced arthritis (33), colitis (34), EAE (35), allergy (36) and transplantation (16). However it was recently reported that CD4 + iTregs are not stable in vivo and failed in preventing acute GVHD in the B6-to-BALB/c model (8, 9).…”

Section: Discussionmentioning

confidence: 99%

TGF-β–Induced CD4+Foxp3+ T Cells Attenuate Acute Graft-versus-Host Disease by Suppressing Expansion and Killing of Effector CD8+ Cells

Lü

Chen

et al. 2014

The Journal of Immunology

Self Cite

View full text Add to dashboard Cite

TGF-β-induced CD4+Foxp3+ T cells (iTregs) have been identified as important prevention and treatment strategies for cell therapy in autoimmune diseases and other disorders. However, the potential use of iTregs as a treatment modality for acute graft-verse-host disease (GVHD) has not been realized because iTregs may be unstable and less suppressive in this disease. Here we restudied the ability of iTregs to prevent and treat acute GVHD in two different mouse models. Our results showed that so long as an appropriate iTreg-generation protocol is used, these iTregs consistently displayed a potent ability to control acute GVHD development and reduce mortality in the acute GVHD animal models. iTreg infusion markedly suppressed the engraftment of donor CD8+ cells and CD4+ cells, the expression of Granzyme A and B, the cytotoxic effect of donor CD8+ cells and the production of T cell cytokines in acute GVHD. We therefore conclude that so long as the right methods for generating iTreg cells have been employed, iTregs can indeed prevent and even treat acute GVHD.

show abstract

Induced CD4+ forkhead box protein–positive T cells inhibit mast cell function and established contact hypersensitivity through TGF-β1

Cited by 53 publications

References 59 publications

Neutrophil–Endothelial Interactions Mediate Angiopoietin-2–Associated Pulmonary Endothelial Cell Dysfunction in Indirect Acute Lung Injury in Mice

Neutrophil–Endothelial Interactions Mediate Angiopoietin-2–Associated Pulmonary Endothelial Cell Dysfunction in Indirect Acute Lung Injury in Mice

Doxycycline exerts multiple anti-allergy effects to attenuate murine allergic conjunctivitis and systemic anaphylaxis

TGF-β–Induced CD4+Foxp3+ T Cells Attenuate Acute Graft-versus-Host Disease by Suppressing Expansion and Killing of Effector CD8+ Cells

Contact Info

Product

Resources

About