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Setting up TRAPS.

Tom Pettersson¹, Jonas Kantonen, Sampsa Matikainen

¹Department of Medicine, University of Helsinki and Helsinki University Central Hospital, Haartmaninkatu 4, Helsinki, Finland. tom.pettersson@hus.fi

Annals of Medicine

|February 3, 2011

Summary

This summary is machine-generated.

Tumour necrosis factor (TNF) receptor-associated periodic syndrome (TRAPS) is an inherited autoinflammatory disorder. Misfolded TNFR1 receptors trapped in the endoplasmic reticulum cause inflammation, leading to recurrent fevers and potential amyloidosis.

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Area of Science:

Genetics and Immunology
Molecular Biology
Clinical Medicine

Background:

Tumour necrosis factor (TNF) receptor-associated periodic syndrome (TRAPS) is a dominantly inherited autoinflammatory disease.
It is caused by mutations in the TNFRSF1A gene, encoding TNF receptor 1 (TNFR1).
TRAPS presents with recurrent fevers, abdominal pain, rash, and can lead to AA amyloidosis.

Purpose of the Study:

To review the current understanding of TRAPS pathogenesis.
To integrate recent clinical and laboratory data.
To elucidate the mechanisms behind the hyperinflammatory phenotype.

Main Methods:

Review of existing clinical and laboratory studies on TRAPS.
Analysis of genetic mutations in TNFRSF1A.
Investigation of protein misfolding and endoplasmic reticulum retention.

Main Results:

Mutated TNFR1 receptors are often misfolded and retained in the endoplasmic reticulum.
This intracellular retention triggers an inflammatory response and cytokine production.
TNFα-dependent signaling appears defective, despite the hyperinflammatory state.

Conclusions:

Endoplasmic reticulum retention of misfolded TNFR1 is a key pathogenic mechanism in TRAPS.
This leads to constitutive pro-inflammatory cytokine expression.
Interleukin-1 blockade may be more effective than TNF blockade therapeutically.