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Related Concept Videos

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T cells are integral to our adaptive immune system, recognizing and effectively responding to foreign antigens. T cell activation and clonal selection are pivotal in orchestrating this immune response. This article elucidates these mechanisms, detailing the roles of cluster of differentiation (CD) markers, major histocompatibility complex (MHC) molecules, costimulatory signals, and the process of clonal selection.
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The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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The T and B lymphocytes of the adaptive immune system develop from common lymphoid progenitor cells in the bone marrow. These progenitors give rise to precursors that eventually develop into both T and B lymphocytes. As these precursors mature, they gain the ability to detect and respond to foreign antigens in the body, a process known as immunocompetence. Additionally, these precursors acquire self-tolerance, a process that ensures they do not react to self-antigens. This intricate system...
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BPTF Is Essential for T Cell Homeostasis and Function.

Bing Wu1,2, Yunqi Wang1,2, Chaojun Wang1,2,3

  • 1Lineberger Comprehensive Cancer Center, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599.

Journal of Immunology (Baltimore, Md. : 1950)
|November 2, 2016
PubMed
Summary
This summary is machine-generated.

Bromodomain PHD finger transcription factor (BPTF) is crucial for maintaining T cell homeostasis and regulatory T (Treg) cell function. Deleting BPTF impairs Treg cells, leading to autoimmunity and reduced Foxp3 expression.

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Area of Science:

  • Immunology
  • Epigenetics
  • Molecular Biology

Background:

  • Bromodomain PHD finger transcription factor (BPTF) is an ATP-dependent chromatin remodeler vital for gene regulation.
  • While its role in early T cell development is known, BPTF's function in mature T cells and regulatory T cells (Tregs) is unclear.

Purpose of the Study:

  • To investigate the function of BPTF in mature T cells and regulatory T cells (Tregs).
  • To determine the role of BPTF in maintaining immune homeostasis.

Main Methods:

  • Specific deletion of BPTF in late-stage developing T cells.
  • Analysis of T cell homeostasis, Treg cell maintenance, and Foxp3 expression.
  • Assessment of lymphocyte infiltration and systemic autoimmunity.

Main Results:

  • BPTF is critical for T cell homeostasis in a cell-intrinsic manner.
  • BPTF is essential for the maintenance and function of Treg cells.
  • Treg-specific BPTF deletion caused reduced Foxp3, increased organ infiltration, and autoimmune syndrome.

Conclusions:

  • BPTF plays a vital role in mature T cell and Treg cell function.
  • BPTF is essential for maintaining immune homeostasis.
  • Disruption of BPTF in Tregs leads to autoimmune disease.