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Related Concept Videos

T Cell Activation and Clonal Selection01:22

T Cell Activation and Clonal Selection

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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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Renewal of Intestinal Stem Cells01:23

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The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the...
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Cancer Stem Cells and Tumor Maintenance02:40

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Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
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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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Tumor Progression02:07

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Tumor progression is a phenomenon where the pre-formed tumor acquires successive mutations to become clinically more aggressive and malignant. In the 1950s, Foulds first described the stepwise progression of cancer cells through successive stages.
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Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
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T-cell Subset Features and Distributions Evolve across the Colorectal Precancer-Cancer Spectrum.

Yasutoshi Takashima1, Andressa Dias Costa1, Naohiko Akimoto2,3

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T-cell infiltration differs across colorectal cancer precursors and invasive tumors. Serrated lesions show more intraepithelial T-cells, while precursors generally have higher T-cell densities than carcinomas.

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Area of Science:

  • Oncology
  • Immunology
  • Gastroenterology

Background:

  • The immune microenvironment is key in colorectal cancer (CRC) but poorly understood in precursors.
  • T-cell infiltrates may vary across the colorectal neoplastic spectrum.

Purpose of the Study:

  • To investigate T-cell infiltration patterns in colorectal carcinoma precursors versus invasive CRC.
  • To understand immune microenvironment evolution during CRC development.

Main Methods:

  • Analyzed 1,825 tissue specimens (precursors and carcinomas) using multispectral immunofluorescence for T-cell markers (CD3, CD4, CD8, FOXP3, CD45RA, CD45RO).
  • Applied supervised machine learning to quantify T-cell phenotypes (naive, memory, regulatory).

Main Results:

  • Precursors generally had higher CD3+CD4+ and CD3+CD8+ cell densities than invasive CRC.
  • Serrated lesions (hyperplastic polyps, sessile serrated lesions) showed increased intraepithelial CD3+CD8+ cells.
  • Greater villous component in adenomas correlated with fewer intraepithelial CD3+CD8+ cells.

Conclusions:

  • T-cell infiltration patterns significantly vary across the colorectal neoplastic spectrum.
  • Immune microenvironment composition changes during precursor progression to CRC.