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Related Concept Videos

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...
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Hypersensitivity Reactions: Delayed Hypersensitivity Reactions01:29

Hypersensitivity Reactions: Delayed Hypersensitivity Reactions

Delayed-Type Hypersensitivity (DTH), or Type IV hypersensitivity, is a cell-mediated immune response. It occurs when T cells, rather than antibodies, mediate a reaction to specific antigens. It is characterized by a delayed onset (1-2 days) and involves the recruitment of macrophages to the inflammation site.The initiation of a DTH response begins with the sensitization of T cells. During this phase, which lasts at least 1-2 weeks, antigen-specific T cells are activated, clonally expanded, and...
Immune Response Against Viral Pathogens01:29

Immune Response Against Viral Pathogens

The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
Acute Kidney Injury II: Pathophysiology01:29

Acute Kidney Injury II: Pathophysiology

Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
T Cell Activation and Clonal Selection01:22

T Cell Activation and Clonal Selection

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.
Naive T cells that have not yet encountered an antigen express two primary CD...

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Related Experiment Video

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In Vitro Differentiation of Naive CD4+ T Cells into Pathogenic Th17 Cells in Mouse
07:46

In Vitro Differentiation of Naive CD4+ T Cells into Pathogenic Th17 Cells in Mouse

Published on: October 25, 2024

Th1 and Th17 cells induce proliferative glomerulonephritis.

Shaun A Summers1, Oliver M Steinmetz, Ming Li

  • 1Centre for Inflammatory Diseases, Monash University Department of Medicine, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria 3168, Australia.

Journal of the American Society of Nephrology : JASN
|October 13, 2009
PubMed
Summary

Both T-helper 1 (Th1) and T-helper 17 (Th17) effector cells can cause proliferative glomerulonephritis, a kidney disease. This study clarifies their distinct roles in disease development, offering insights for targeted therapies.

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Area of Science:

  • Immunology
  • Nephrology
  • Pathogenesis of Glomerulonephritis

Background:

  • T-helper 1 (Th1) effector cells are known to contribute to glomerulonephritis.
  • The role of T-helper 17 (Th17) effector cells in glomerulonephritis pathogenesis remains unclear.

Purpose of the Study:

  • To investigate and compare the involvement of Th1 and Th17 effector cells in inducing antigen-specific glomerulonephritis.
  • To elucidate the distinct mechanisms by which Th1 and Th17 cells mediate glomerular injury.

Main Methods:

  • Utilized a mouse model of antigen-specific glomerulonephritis by sensitizing ovalbumin on the glomerular basement membrane of Rag1(-/-) mice.
  • Administered either Th1- or Th17-polarized ovalbumin-specific CD4+ effector cells to induce kidney injury.
  • Assessed albuminuria, histologic damage (including crescent formation), urinary nitrate levels, and renal gene expression (NOS2, CCL2, CCL5, CXCL1).

Main Results:

  • Both Th1 and Th17 effector cells induced proliferative glomerulonephritis.
  • Th1-injected mice showed progressive albuminuria, crescent formation, elevated urinary nitrate, and increased NOS2, CCL2, and CCL5 mRNA.
  • Th17-injected mice exhibited rapid albuminuria, increased neutrophils, and higher CXCL1 mRNA expression in glomeruli compared to Th1-injected mice.

Conclusions:

  • Th1 and Th17 effector cells are capable of inducing glomerular injury independently.
  • Distinct pathogenic pathways are mediated by Th1 and Th17 cells in proliferative glomerulonephritis.
  • Understanding these subset-specific mechanisms may pave the way for targeted therapeutic strategies for glomerulonephritis.