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Related Concept Videos

Pulmonary Tuberculosis I01:29

Pulmonary Tuberculosis I

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Tuberculosis, often called TB, is a contagious illness primarily caused by Mycobacterium tuberculosis. It mainly affects the lung parenchyma but can also impact other body parts.
Causative Organism
The primary infectious agent causing tuberculosis is Mycobacterium tuberculosis, a slow-growing, acid-fast, aerobic rod that exhibits sensitivity to heat and ultraviolet light. Instances of Mycobacterium bovis and Mycobacterium avium contributing to the development of TB infection are rare.
Mode of...
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Pulmonary Tuberculosis II01:28

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Tuberculosis, or TB, is a bacterial infectious disease caused by Mycobacterium tuberculosis. While its primary impact is on the lungs, leading to pulmonary tuberculosis, it can also affect various other organs, a condition referred to as extrapulmonary tuberculosis.
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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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Pulmonary Tuberculosis IV01:26

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Tuberculosis, more commonly referred to as TB, is an infectious disease stemming from Mycobacterium tuberculosis. While it primarily impacts the lungs, TB can also affect other body areas. Given its severity and global impact, timely and accurate diagnosis is crucial for controlling its spread and improving patient outcomes.
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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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Related Experiment Video

Updated: Apr 27, 2026

Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice
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Altered CD8(+) T cell frequency and function in tuberculous lymphadenitis.

Nathella Pavan Kumar1, Rathinam Sridhar2, Luke Elizabeth Hanna3

  • 1National Institutes of Health-International Center for Excellence in Research, Chennai, India; National Institute for Research in Tuberculosis, Chennai, India.

Tuberculosis (Edinburgh, Scotland)
|July 17, 2014
PubMed
Summary

Tuberculous lymphadenitis (TBL) involves specific CD8(+) T cell responses, with elevated Type 1 and Type 17 cytokines but reduced cytotoxic molecules. These changes are dependent on Interleukin-1 and Interleukin-6 signaling.

Keywords:
CD8 T cellsCytokinesCytotoxic moleculesLymphadenitisTuberculosis

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Area of Science:

  • Immunology
  • Infectious Diseases
  • Cellular Biology

Background:

  • CD8(+) T cells secreting Type 1 and Type 17 cytokines are crucial for immunity against pulmonary tuberculosis (PTB).
  • The specific role of these CD8(+) T cells in tuberculous lymphadenitis (TBL) remains less understood.
  • Understanding TBL pathogenesis requires detailed analysis of CD8(+) T cell subsets and their functions.

Purpose of the Study:

  • To investigate the distribution and function of CD8(+) T cells expressing Type 1, Type 2, and Type 17 cytokines and cytotoxic molecules in TBL.
  • To compare immune responses in TBL patients with those suffering from PTB.
  • To elucidate the role of Interleukin-1 (IL-1) and Interleukin-6 (IL-6) in TBL pathogenesis.

Main Methods:

  • Analysis of whole blood immune responses in individuals with PTB and TBL.
  • Measurement of baseline and mycobacterial-antigen specific CD8(+) T cell cytokine and cytotoxic molecule expression.
  • In vitro blockade of IL-1 receptor (IL-1R) and IL-6 receptor (IL-6R) during antigenic stimulation.

Main Results:

  • TBL patients showed higher frequencies of CD8(+) T cells expressing Type 1 (IL-2, TNFα) and Type 17 (IL-17A, IL-17F) cytokines compared to PTB patients.
  • TBL patients had reduced frequencies of CD8(+) T cells expressing cytotoxic molecules like perforin, granzyme B, and CD107a.
  • Blocking IL-1R and IL-6R significantly decreased Type 1 and Type 17 cytokine-producing CD8(+) T cells in TBL.

Conclusions:

  • TBL is characterized by an expansion of CD8(+) T cells producing Type 1 and Type 17 cytokines, dependent on IL-1 and IL-6.
  • Altered frequencies of cytotoxic molecules on CD8(+) T cells are observed in TBL.
  • These CD8(+) T cell profiles are significantly associated with the pathogenesis of TBL.