Jove
Visualize
Contact Us

Related Concept Videos

Antigens Involved in Adaptive Immunity01:26

Antigens Involved in Adaptive Immunity

1.7K
An antigen is any substance the immune system identifies as foreign and potentially harmful to the body, prompting an immune response. Antigens have two functional properties: immunogenicity and reactivity. Immunogenicity is the ability of an antigen to stimulate a specific immune response. At the same time, reactivity describes the antigen's ability to react with the cells and antibodies produced in response to it.
Complete Antigens
Complete antigens possess both immunogenicity and...
1.7K
T Cell Types and Functions01:24

T Cell Types and Functions

3.2K
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...
3.2K
Immunodeficiency Diseases01:25

Immunodeficiency Diseases

3.7K
Immunodeficiency disorders are conditions in which the immune system's ability to fight infectious disease and cancer is compromised or entirely absent. The immune system comprises a complex network of cells, tissues, and organs that work together to protect the body from potentially harmful invaders. When this system is deficient or not functioning properly, it leaves the body susceptible to infections, diseases, or other complications.
There are three main causes of immunodeficiency...
3.7K
Type I Diabetes I: Introduction01:12

Type I Diabetes I: Introduction

45
Type 1 diabetes mellitus is a chronic metabolic disorder characterized by an absolute deficiency of insulin resulting from the autoimmune destruction of pancreatic β-cells. Although it can occur at any age, it is most commonly diagnosed in childhood, adolescence, or early adulthood. The loss of insulin production impairs cellular glucose uptake, resulting in persistent hyperglycemia and necessitating lifelong insulin therapy.Autoimmune Destruction of β-CellsThe hallmark of type 1...
45
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

75
Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular...
75
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

35
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...
35

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Editorial Expression of Concern: DOCK8 functions as an adaptor that links TLR-MyD88 signaling to B cell activation.

Nature immunology·2026
Same author

The role of dupilumab in the treatment of eosinophilic esophagitis.

Immunotherapy·2024
Same author

A Novel Combination of Compound Heterozygous Variants in IFNGR1 Causing Complete IFNGR1 Deficiency.

Journal of clinical immunology·2024
Same author

Inborn Errors of the Immune System Associated With Atopy.

Frontiers in immunology·2022
Same author

Author Correction: DOCK8 functions as an adaptor that links TLR-MyD88 signaling to B cell activation.

Nature immunology·2022
Same author

Immune dysregulation and multisystem inflammatory syndrome in children (MIS-C) in individuals with haploinsufficiency of SOCS1.

The Journal of allergy and clinical immunology·2020
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Video

Updated: Apr 30, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
12:59

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 27, 2013

33.7K

TH17 deficiency in human disease.

Douglas R McDonald1

  • 1Division of Immunology, Children's Hospital, Boston and Harvard Medical School, Boston, MA 02115, USA. douglas.mcdonald@childrens.harvard.edu

The Journal of Allergy and Clinical Immunology
|May 5, 2012
PubMed
Summary
This summary is machine-generated.

Naive T cells differentiate into effector T cells for immunity. T(H)17 cells, crucial for fungal defense, develop upon Candida species activation, as seen in chronic mucocutaneous candidiasis patients.

More Related Videos

Th17 Inflammation Model of Oropharyngeal Candidiasis in Immunodeficient Mice
08:02

Th17 Inflammation Model of Oropharyngeal Candidiasis in Immunodeficient Mice

Published on: February 18, 2015

9.0K
Author Spotlight: Achieving High-Purity In Vitro Differentiation of Th17 Cells Using Cytokine Concentration Modulation
07:46

Author Spotlight: Achieving High-Purity In Vitro Differentiation of Th17 Cells Using Cytokine Concentration Modulation

Published on: October 25, 2024

3.2K

Related Experiment Videos

Last Updated: Apr 30, 2026

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes
12:59

Isolation and Th17 Differentiation of Naïve CD4 T Lymphocytes

Published on: September 27, 2013

33.7K
Th17 Inflammation Model of Oropharyngeal Candidiasis in Immunodeficient Mice
08:02

Th17 Inflammation Model of Oropharyngeal Candidiasis in Immunodeficient Mice

Published on: February 18, 2015

9.0K
Author Spotlight: Achieving High-Purity In Vitro Differentiation of Th17 Cells Using Cytokine Concentration Modulation
07:46

Author Spotlight: Achieving High-Purity In Vitro Differentiation of Th17 Cells Using Cytokine Concentration Modulation

Published on: October 25, 2024

3.2K

Area of Science:

  • Immunology
  • Microbiology

Background:

  • T cell differentiation is vital for immunity against pathogens.
  • Candida species activate innate immune responses, guiding T cell development.
  • T(H)17 cells are essential for mucosal immunity, particularly against fungal infections.

Purpose of the Study:

  • To investigate the role of T(H)17 cells in host defense against Candida species.
  • To understand the development of T(H)17 cells in response to fungal infections.
  • To analyze patient cohorts with T(H)17 deficiency and chronic mucocutaneous candidiasis.

Main Methods:

  • Analysis of patient cohorts with T(H)17 deficiency.
  • Investigating the role of pattern-recognition receptors in innate immune activation.
  • Studying the differentiation pathways of naive T cells.

Main Results:

  • T(H)17 cells are critical for host defense against Candida species.
  • T(H)17 deficiency leads to susceptibility to chronic mucocutaneous candidiasis.
  • Insights into the complex mechanisms of T(H)17 cell development were gained.

Conclusions:

  • T(H)17 cells and their cytokines play a significant role in human immunity against fungi.
  • Understanding T(H)17 cell development is key to addressing fungal infections and immune deficiencies.