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Open AccessJournal ArticleDOI

Treg cells expressing the coinhibitory molecule TIGIT selectively inhibit proinflammatory Th1 and Th17 cell responses.

TLDR
TIGIT expression identifies a Treg cell subset that demonstrates selectivity for suppression of Th1 and Th17 cell but not Th2 cell responses.
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This article is published in Immunity.The article was published on 2014-04-17 and is currently open access. It has received 636 citations till now. The article focuses on the topics: TIGIT & FOXP3.

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Citations
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Lag-3, Tim-3, and TIGIT: Co-inhibitory Receptors with Specialized Functions in Immune Regulation

TL;DR: Co-inhibitory receptors, such as CTLA-4 and PD-1, have an important role in regulating T cell responses and have proven to be effective targets in the setting of chronic diseases where constitutive co- inhibitory receptor expression on T cells dampens effector T-cell responses.
Journal ArticleDOI

The immunology of asthma

TL;DR: Results from in-depth molecular studies of mouse models in light of the results from the first clinical trials targeting key cytokines in humans are discussed and the extraordinary heterogeneity of asthma is described.
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Single-Cell Map of Diverse Immune Phenotypes in the Breast Tumor Microenvironment.

TL;DR: A preprocessing pipeline, SEQC, and a Bayesian clustering and normalization method, Biscuit, are developed to address computational challenges inherent to single-cell data and support a model of continuous activation in T cells and do not comport with the macrophage polarization model in cancer.
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Coinhibitory Pathways in Immunotherapy for Cancer.

TL;DR: The immunoregulatory functions of coinhibitory pathways and their translation to effective immunotherapies for cancer are discussed and blockade of the PD-1 and CTLA-4 checkpoints is proving to be an effective and durable cancer immunotherapy in a subset of patients.
References
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Journal ArticleDOI

Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells.

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.
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Interleukin-10-deficient mice develop chronic enterocolitis

TL;DR: The results indicate that the bowel inflammation in the mutants originates from uncontrolled immune responses stimulated by enteric antigens and that IL-10 is an essential immunoregulator in the intestinal tract.
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CD4+CD25+ Immunoregulatory T Cells Suppress Polyclonal T Cell Activation In Vitro by Inhibiting Interleukin 2 Production

TL;DR: Data support the concept that the CD4+CD25+ T cells in normal mice may represent a distinct lineage of “professional” suppressor cells.
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CTLA-4 Control over Foxp3+ Regulatory T Cell Function

TL;DR: It is shown that a specific deficiency of cytotoxic T lymphocyte antigen 4 (CTLA-4) in Tregs results in spontaneous development of systemic lymphoproliferation, fatal T cell–mediated autoimmune disease, and hyperproduction of immunoglobulin E in mice.
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