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TRAPS mutations in Tnfrsf1a decrease the responsiveness to TNFα via reduced cell surface expression of TNFR1.

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TRAPS mutations in TNFRSF1A did not increase inflammation in mice. Instead, these mutations suppressed TNFα responses by reducing cell surface TNFR1, suggesting unconfirmed factors cause TRAPS-associated inflammation.

Keywords:
TNF receptor 1TNF receptor-associated periodic syndromeautoinflammatory diseasemurine modeltumor necrosis factor-α

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Area of Science:

  • Immunology
  • Genetics
  • Rheumatology

Background:

  • Tumor necrosis factor (TNF) receptor-associated periodic syndrome (TRAPS) is an autoinflammatory disease linked to mutations in TNFRSF1A.
  • Previous studies on TRAPS mechanisms used in vitro overexpression models, potentially yielding artificial results.
  • Reproducing TRAPS mutations at physiological levels is crucial but limited.

Purpose of the Study:

  • To generate and analyze TRAPS mutant mice to understand the in vivo and in vitro inflammatory responses.
  • To investigate the effect of specific TNFRSF1A mutations (T79M, G87V, T90I) on inflammatory phenotypes.

Main Methods:

  • Generated three Tnfrsf1a mutant mouse strains (T79M, G87V, T90I).
  • Analyzed inflammatory phenotypes in mutant mice under standard conditions and after challenge (LPS/D-galactosamine).
  • Crossed mutant mice with human TNFα transgenic mice to study TNFα-mediated arthritis.
  • Assessed inflammatory responses in vitro using primary bone marrow-derived macrophage cultures.

Main Results:

  • No detectable inflammatory phenotypes were observed in mutant mice under standard housing.
  • TRAPS mutant mice (T79M, G87V) showed reduced mortality after LPS/D-galactosamine challenge and suppressed TNFα-mediated arthritis.
  • In vitro, TRAPS mutations attenuated TNFα responses but not LPS responses in macrophages, linked to decreased cell surface TNFR1 expression.

Conclusions:

  • TRAPS mutations do not augment TNFα or LPS inflammatory responses; they suppress TNFα responsiveness.
  • Decreased cell surface TNFR1 expression is implicated in the suppressed TNFα response.
  • TRAPS-associated inflammation may be driven by currently unidentified disease-specific proinflammatory factors.