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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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Staphylococcus aureus and Hyper-IgE Syndrome.

Bonggoo Park¹, George Y Liu²

¹Division of Pediatric Infectious Diseases and the Immunobiology Research Institute, Cedars Sinai Medical Center, Los Angeles, CA 90048, USA.

International Journal of Molecular Sciences

|December 4, 2020

Summary

Signal transducer and activator of transcription 3 (STAT3) mutations cause Hyper-immunoglobulin E syndrome (HIES), leading to recurrent Staphylococcus aureus infections. These STAT3 mutations disrupt T helper 17 cell differentiation and IL-17/IL-22 production, impairing host defense.

Keywords:

Staphylococcus aureus T helper 17 (TH17) cell antimicrobial peptides chemokines hyper-immunoglobulin E syndrome (HIES)primary immunodeficiency disease signal transducer and activator of transcription 3 staphylococcal lung and skin infections

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Area of Science:

Immunology
Genetics
Dermatology

Background:

Hyper-immunoglobulin E syndrome (HIES) is a primary immunodeficiency.
HIES presents with recurrent Staphylococcus aureus infections, eczema, and skeletal issues.
High serum immunoglobulin E levels are a hallmark of HIES.

Purpose of the Study:

To elucidate the genetic basis of Hyper-immunoglobulin E syndrome (HIES).
To understand the molecular mechanisms underlying HIES pathogenesis.
To explain the recurrent S. aureus infections in HIES patients.

Main Methods:

Genetic studies identifying mutations in the STAT3 gene.
Analysis of STAT3 mutation localization within functional domains.
Investigation of T helper 17 cell differentiation and cytokine production (IL-17, IL-22).

Main Results:

Dominant-negative mutations in the STAT3 gene cause sporadic and dominant HIES.
STAT3 mutations disrupt T helper 17 cell differentiation and IL-17/IL-22 expression.
Deficiency in IL-17 and IL-22 impairs epithelial cell anti-staphylococcal defenses.

Conclusions:

STAT3 mutations are the primary cause of HIES.
Impaired T helper 17 immunity explains S. aureus susceptibility in HIES.
Understanding STAT3's role offers insights into immunodeficiency and host defense.