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Related Concept Videos

Inflammatory Response01:28

Inflammatory Response

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.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
T Cell Types and Functions01:24

T Cell Types and Functions

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.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

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.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
Defense Against Bacterial Pathogens01:31

Defense Against Bacterial Pathogens

The human immune system is a complex network of cells, tissues, and organs that work together to defend the body against bacterial infections. It consists of various immune cells, each playing a specific role in the defense mechanism.
Phagocytes
Phagocytes are the frontline soldiers of the immune system. They include neutrophils and macrophages. Neutrophils are the most abundant type of white blood cell and are quickly mobilized to the site of infection. Macrophages are larger cells that patrol...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...

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Related Experiment Video

Updated: Jun 11, 2026

Characterization of Immune Cells and Proinflammatory Mediators in the Pulmonary Environment
09:00

Characterization of Immune Cells and Proinflammatory Mediators in the Pulmonary Environment

Published on: June 24, 2020

Eicosanoid pathways regulate adaptive immunity to Mycobacterium tuberculosis.

Maziar Divangahi1, Danielle Desjardins, Cláudio Nunes-Alves

  • 1Division of Rheumatology, Immunology, and Allergy, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Nature Immunology
|July 13, 2010
PubMed
Summary
This summary is machine-generated.

Mycobacterium tuberculosis infection hinders apoptosis and promotes necrosis, preventing T cell immunity. Activating the 5-lipoxygenase pathway by M. tuberculosis impedes antigen presentation, delaying crucial early immune responses.

Related Experiment Videos

Last Updated: Jun 11, 2026

Characterization of Immune Cells and Proinflammatory Mediators in the Pulmonary Environment
09:00

Characterization of Immune Cells and Proinflammatory Mediators in the Pulmonary Environment

Published on: June 24, 2020

Area of Science:

  • Immunology
  • Microbiology
  • Cell Biology

Background:

  • Macrophages are key in immunity against Mycobacterium tuberculosis (M. tuberculosis).
  • M. tuberculosis manipulates host cell death pathways, favoring necrosis for spread over apoptosis, which limits bacterial viability.
  • Virulent M. tuberculosis actively inhibits apoptosis and promotes necrosis by suppressing prostaglandin E(2) production.

Purpose of the Study:

  • To investigate the role of the 5-lipoxygenase pathway in M. tuberculosis-induced immune evasion.
  • To understand how M. tuberculosis interferes with antigen presentation by dendritic cells.
  • To elucidate the mechanisms behind delayed T cell immunity during M. tuberculosis infection.

Main Methods:

  • Analysis of host cell death pathways (apoptosis vs. necrosis) in infected macrophages.
  • Investigation of the 5-lipoxygenase pathway activation by M. tuberculosis.
  • Assessment of antigen cross-presentation by dendritic cells in the presence of M. tuberculosis.

Main Results:

  • M. tuberculosis activates the 5-lipoxygenase pathway in infected macrophages.
  • This pathway activation inhibits apoptosis and prevents antigen cross-presentation by dendritic cells.
  • Impeded antigen presentation leads to delayed initiation of T cell-mediated immunity.

Conclusions:

  • M. tuberculosis utilizes the 5-lipoxygenase pathway to evade host immune responses.
  • Inhibition of apoptosis and impaired antigen presentation are critical mechanisms for M. tuberculosis virulence.
  • Targeting these pathways could enhance early T cell immunity against M. tuberculosis.