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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...
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Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum sickness, a systemic...
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Recognition of Epidermal Transglutaminase by IgA and Tissue Transglutaminase 2 Antibodies in a Rare Case of Rhesus Dermatitis
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Pathogenesis of hyper IgE syndrome.

Jennifer Heimall1, Alexandra Freeman, Steven M Holland

  • 1Laboratory of Clinical Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892-1684, USA.

Clinical Reviews in Allergy & Immunology
|May 20, 2009
PubMed
Summary

Hyper IgE syndrome (HIES) involves immune, connective, and skeletal issues due to STAT3 mutations. Understanding these genetic defects offers new treatment avenues for HIES and common related conditions.

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Area of Science:

  • Immunology
  • Genetics
  • Molecular Biology

Background:

  • Hyper IgE syndrome (HIES) is a primary immunodeficiency marked by high IgE, eosinophilia, eczema, and infections.
  • Autosomal dominant HIES stems from STAT3 mutations, causing inflammation, and connective/skeletal issues.

Purpose of the Study:

  • To elucidate the pathophysiology of HIES, particularly the role of STAT3 mutations.
  • To explore potential new treatments for HIES and associated common conditions.

Main Methods:

  • Analysis of STAT3 mutations in autosomal dominant HIES.
  • Utilizing animal models with tissue-specific STAT3 deficiency.
  • Examining cytokine and transcriptional array data.
  • Detailed clinical phenotyping of patients.

Main Results:

  • STAT3 mutations explain some immunological and non-immunological abnormalities in AD-HIES.
  • Identified links between HIES and common conditions like staphylococcal infections, scoliosis, osteoporosis, bronchiectasis, and arterial aneurysms.
  • Characterization of STAT3 deficiency genotypes may reveal genotype-phenotype correlations.

Conclusions:

  • Further understanding of STAT3's role in HIES pathophysiology can lead to improved treatments.
  • Investigating autosomal recessive forms of HIES is crucial for a complete picture.
  • Insights into HIES mechanisms can advance somatic and immune biology, improving patient outcomes.