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Related Concept Videos

Asthma I: Introduction01:28

Asthma I: Introduction

Asthma is a chronic inflammatory disorder of the airways characterized by variable airflow obstruction and heightened bronchial responsiveness to a wide range of triggers. The underlying inflammation leads to airway swelling, mucus hypersecretion, and smooth muscle constriction, all of which narrow the airway lumen and impede airflow. Clinically, asthma presents with recurrent episodes of wheezing, shortness of breath, chest tightness, and coughing, symptoms that typically vary in intensity and...
Asthma-II: Pathophysiology and Classification01:26

Asthma-II: Pathophysiology and Classification

Asthma is a prevalent chronic respiratory condition marked by inflammation and hyperresponsiveness of the airways. Its pathophysiology involves complex interactions among inflammatory pathways, immune responses, and neural mechanisms.
Additionally, environmental and genetic factors play crucial roles in determining an individual's susceptibility to asthma and the severity of their condition.
Critical processes in asthma pathophysiology include:
Asthma: Pathogenesis and Management01:20

Asthma: Pathogenesis and Management

Asthma is a chronic pulmonary condition involving inflammation of the airways, hyper-reactivity, and reversible obstruction of the airways. This condition can significantly impact a person's quality of life, making breathing difficult and leading to distressing symptoms.
Asthma is classified as allergic and non-allergic. Allergens such as dust mites, pollen, and pet dander trigger allergic asthma, while factors like cold air, intense emotions, or exercise can induce non-allergic asthma.
Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features01:24

Chronic Obstructive Pulmonary Disease III: Chronic Bronchitis Features

Chronic bronchitis is a key phenotype of chronic obstructive pulmonary disease (COPD), characterized by airway-centered inflammation and mucus overproduction. It develops from long-term exposure to harmful particles or gases, most commonly cigarette smoke, which triggers a persistent inflammatory response.Cellular and Structural ChangesInflammation initially affects the large bronchi and later the smaller airways, with infiltration by immune cells, including neutrophils, macrophages, and...
Chronic Obstructive Pulmonary Disease-II: Pathophysiology01:20

Chronic Obstructive Pulmonary Disease-II: Pathophysiology

Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
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...

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Related Experiment Video

Updated: Jun 16, 2026

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy
10:39

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy

Published on: April 16, 2019

TH17 cells in asthma and COPD.

John F Alcorn1, Christopher R Crowe, Jay K Kolls

  • 1Department of Pediatrics, Division of Pulmonology, Children's Hospital of Pittsburgh of UPMC, Pittsburgh, PA 15201, USA. john.alcorn@chp.edu

Annual Review of Physiology
|February 13, 2010
PubMed
Summary
This summary is machine-generated.

Asthma and COPD share immune pathways. T(H)17 cells may drive severe asthma and COPD by promoting inflammation, offering new therapeutic targets for these obstructive lung diseases.

Related Experiment Videos

Last Updated: Jun 16, 2026

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy
10:39

Advanced Imaging of Lung Homing Human Lymphocytes in an Experimental In Vivo Model of Allergic Inflammation Based on Light-sheet Microscopy

Published on: April 16, 2019

Area of Science:

  • Immunology
  • Pulmonology
  • Cellular Biology

Background:

  • Asthma and COPD are chronic obstructive lung diseases with shared immunological mechanisms.
  • Asthma involves airway hyperresponsiveness and inflammation; COPD features emphysematous changes and lymphoid follicles in advanced stages.
  • Current asthma treatments are limited, with severe cases showing steroid resistance linked to neutrophilic inflammation.

Purpose of the Study:

  • To explore the immunological mechanisms underlying asthma and COPD.
  • To investigate the role of T(H)17 cells in neutrophilic and macrophage inflammation in severe asthma and COPD.
  • To identify potential therapeutic targets for steroid-insensitive asthma and COPD.

Main Methods:

  • Review of existing literature on asthma and COPD immunology.
  • Analysis of studies investigating T(H)17 cell function in lung inflammation.
  • Correlation of neutrophilic inflammation with steroid resistance in severe asthma.

Main Results:

  • Advanced COPD exhibits lymphoid follicles, highlighting immunological involvement.
  • T(H)17 cells regulate neutrophilic and macrophage inflammation in the lung.
  • Neutrophilic inflammation is associated with steroid-resistant asthma.

Conclusions:

  • T(H)17 cells are implicated in the pathogenesis of severe, steroid-insensitive asthma and COPD.
  • Understanding the role of neutrophils, macrophages, and T(H)17 cells is crucial for developing new treatments.
  • Shared immunological pathways suggest potential for cross-disease therapeutic strategies.