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T-bet: a bridge between innate and adaptive immunity.

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TLDR
T-bet has a fundamental role in coordinating type 1 immune responses by controlling a network of genetic programmes that regulate the development of certain immune cells and the effector functions of others.
Abstract
Originally described over a decade ago as a T cell transcription factor regulating T helper 1 cell lineage commitment, T-bet is now recognized as having an important role in many cells of the adaptive and innate immune system. T-bet has a fundamental role in coordinating type 1 immune responses by controlling a network of genetic programmes that regulate the development of certain immune cells and the effector functions of others. Many of these transcriptional networks are conserved across innate and adaptive immune cells and these shared mechanisms highlight the biological functions that are regulated by T-bet.

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Cytokines in inflammatory bowel disease

TL;DR: The role of cytokines produced by innate and adaptive immune cells, as well as their relevance to the future therapy of IBD are discussed.
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MAP Kinase Inhibition Promotes T Cell and Anti-tumor Activity in Combination with PD-L1 Checkpoint Blockade.

TL;DR: It is shown that despite the central importance of the MAP kinase pathway in some aspects of T cell function, MEK-targeted agents can be compatible with T-cell-dependent immunotherapy.
Journal ArticleDOI

Model-based assessment of the Role of Uneven Partitioning of Molecular Content on Heterogeneity and Regulation of Differentiation in CD8 T-cell Immune Responses

TL;DR: It is shown that immune response dynamics can be explained by the molecular-content heterogeneity generated by uneven partitioning at cell division, and that the degree of unevenness of molecular partitioning affects the outcome of the immune response and can promote the generation of memory cells.
Journal ArticleDOI

Canonical and Non-Canonical Aspects of JAK–STAT Signaling: Lessons from Interferons for Cytokine Responses

TL;DR: The contribution of non-canonical JAK-STAT signaling to the innate antimicrobial immunity imparted by interferon (IFN) is discussed in this paper. But, the contribution is limited to the activation of the JAK signal.
References
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Journal ArticleDOI

A novel transcription factor, T-bet, directs Th1 lineage commitment.

TL;DR: T-bet initiates Th1 lineage development from naive Thp cells both by activating Th1 genetic programs and by repressing the opposing Th2 programs, as evidenced by the simultaneous induction of IFNgamma and repression of IL-4 and IL-5.
Journal ArticleDOI

Master Transcription Factors and Mediator Establish Super-Enhancers at Key Cell Identity Genes

TL;DR: In this article, the ESC master transcription factors form unusual enhancer domains at most genes that control the pluripotent state, called super-enhancers, which consist of clusters of enhancers that are densely occupied by the master regulators and Mediator.
Journal ArticleDOI

The Transcription Factor GATA-3 Is Necessary and Sufficient for Th2 Cytokine Gene Expression in CD4 T Cells

TL;DR: In transgenic mice, elevated GATA-3 in CD4 T cells caused Th2 cytokine gene expression in developing Th1 cells, indicating that Gata-3 is necessary and sufficient for Th2inflammatory gene expression.

Master Transcription Factors and Mediator Establish Super-Enhancers at Key Cell Identity Genes

TL;DR: It is reported here that the ESC master transcription factors form unusual enhancer domains at most genes that control the pluripotent state, which consist of clusters of enhancers that are densely occupied by the master regulators and Mediator.
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