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Related Concept Videos

Autoimmune Disorders01:29

Autoimmune Disorders

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Autoimmune diseases are a group of disorders in which the body's immune system mistakenly attacks its own cells, tissues, and organs. This results from an overactive immune response against substances and tissues normally present in the body. Let's delve into the concept and mechanism of autoimmune diseases from an immune system point of view, explore different causes and examples of such diseases, and discuss potential solutions.
Concept and Mechanism of Autoimmune Diseases
The immune...
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Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

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Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
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Hypersensitivities01:30

Hypersensitivities

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Hypersensitivity, also known as a hypersensitivity reaction or allergic reaction, is a condition where the body's immune system reacts abnormally to a foreign substance. Such substances, that cause hypersensitivity are referred to as an allergen, could be something typically harmless to most people, like pollen or certain foods.
Types of Hypersensitivities
Hypersensitivity reactions are categorized into four types: Type 1, Type 2, Type 3, and Type 4. Each type has a distinct mechanism...
569
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.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
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What is the Immune System?01:38

What is the Immune System?

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Related Experiment Video

Updated: Jun 19, 2025

Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis
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A TNIP1-driven systemic autoimmune disorder with elevated IgG4.

Arti Medhavy1, Vicki Athanasopoulos1, Katharine Bassett1

  • 1Division of Immunology and Infectious Disease, John Curtin School of Medical Research, Australian National University, Canberra, Australian Capital Territory, Australia.

Nature Immunology
|July 26, 2024
PubMed
Summary
This summary is machine-generated.

A rare TNIP1 gene variant causes systemic autoimmune disease by disrupting mitochondrial repair and increasing Toll-like receptor 7 (TLR7) signaling. This discovery suggests potential new therapies targeting TLR7 for autoimmune conditions.

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Area of Science:

  • Immunology
  • Genetics
  • Molecular Biology

Background:

  • Systemic autoimmune diseases involve autoantibodies like antinuclear antibodies (ANA) and elevated IgG4.
  • Genetic factors play a crucial role in the development of autoimmune disorders.

Purpose of the Study:

  • To identify the genetic basis of systemic autoimmune disease with ANA and IgG4 elevation.
  • To investigate the functional consequences of a specific TNIP1 variant in autoimmunity.

Main Methods:

  • Whole-exome sequencing in affected kindreds.
  • Generation and analysis of mice with an orthologous TNIP1 variant (Tnip1Q346P).
  • Cellular assays assessing B cell phenotypes, signaling pathways (TLR7, MyD88), and mitochondrial autophagy.

Main Results:

  • An identical ultrarare heterozygous TNIP1Q333P variant was found in patients and segregated with disease.
  • Tnip1Q346P mice exhibited autoimmune phenotypes, including ANA, inflammation, and immune cell expansion.
  • The TNIP1 variant impaired mitochondrial autophagy and MyD88/IRAK1 recruitment to autophagosomes, leading to increased interferon-β production.
  • B cell abnormalities were cell-autonomous and rescued by TLR7 or MyD88 ablation.

Conclusions:

  • TNIP1-mediated autoimmunity may result from impaired autophagosome function, leading to increased TLR7 signaling.
  • Defective mitochondrial clearance and subsequent immune dysregulation are implicated.
  • Targeting TLR7 may offer a therapeutic strategy for TNIP1-associated autoimmune diseases.