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Related Concept Videos

T Cell Types and Functions01:24

T Cell Types and Functions

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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
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T Cell Activation and Clonal Selection01:22

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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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Abnormal Proliferation02:23

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Transdifferentiation, also known as lineage reprogramming, was first discovered by Selman and Kafatos in 1974 in silkmoths. They observed that the moths’ cuticle-producing cells transformed into salt-producing cells. Many such cases of natural transdifferentiation occur in organisms. In humans, pancreatic alpha cells can become beta cells. In newts, the loss of the eye’s lens causes the pigmented epithelial cells to transdifferentiate into the lens cells.
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Related Experiment Video

Updated: Mar 29, 2026

Adenoviral Transduction of Naive CD4 T Cells to Study Treg Differentiation
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Pathological conditions re-shape physiological Tregs into pathological Tregs.

William Y Yang1, Ying Shao1, Jahaira Lopez-Pastrana1

  • 1Centers for Metabolic Disease Research, Cardiovascular Research, and Thrombosis Research, Department of Pharmacology, Temple University School of Medicine, Philadelphia, PA 19140, U.S.A.

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Summary

Regulatory T cells (Tregs) are crucial for immune balance. Recent advancements reveal their plasticity and the shift from physiological to pathological roles, offering new therapeutic targets for immune-related diseases.

Keywords:
epigenetic mechanismshistone modificationsimmune suppressionmetabolic cardiovascular diseasesregulatory T cells

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Area of Science:

  • Immunology
  • Cell Biology

Background:

  • CD4+FOXP3+ regulatory T cells (Tregs) are vital for immune tolerance and regulating inflammatory and autoimmune responses.
  • Significant progress has been made in understanding Treg generation, subsets, tissue specificity, homeostasis, and regulation since their discovery in 1995.

Purpose of the Study:

  • To review eight key recent advancements in Treg research.
  • To introduce the novel concept of "physiological Tregs" transforming into "pathological Tregs" in disease states.

Main Methods:

  • Concise review of existing literature and research findings on Tregs.
  • Analysis of Treg generation, subsets, tissue specificity, homeostasis, regulation, plasticity, and epigenetic control.

Main Results:

  • Innovations in understanding Treg generation, diverse subsets (tTregs, pTregs, iTregs, iTreg35), and tissue-specific roles (central, effector, tissue-resident).
  • Insights into Treg homeostasis, regulation by PAMPs/DAMPs receptors, and remarkable plasticity, including re-differentiation into other T helper subsets (Th1, Th2, Tfh, Th17).
  • Elucidation of epigenetic regulation of Treg phenotypes and functions, and the proposed concept of "physiological Tregs" becoming "pathological Tregs".

Conclusions:

  • Continued advancement in understanding Tregs is critical for developing novel therapeutics.
  • Targeting Tregs holds promise for treating inflammatory diseases, allergies, autoimmune disorders, and cancers.
  • The concept of Treg plasticity and their transition to pathological states offers new avenues for immunomodulatory therapies.