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Expression of the class I interferon-related MxA protein in temporal arteries in polymyalgia rheumatica and temporal

C Nordborg1, K Larsson, P Aman

  • 1Department of Pathology, Sahlgrenska University Hospital, SE-41345 Göteborg, Sweden. claes.nordborg@vgregion.se

Scandinavian Journal of Rheumatology
|January 30, 2009
PubMed
Abstract

Insights

Interferon type I (IFN-I)-associated MxA protein is expressed in arteries of polymyalgia rheumatica (PMR) and temporal arteritis (TA) patients. This suggests IFN-I influences vessel walls in these conditions.

Area of Science:

  • Immunology
  • Rheumatology
  • Vascular Biology

Background:

  • Polymyalgia rheumatica (PMR) and temporal arteritis (TA) are inflammatory conditions affecting the arteries.
  • The role of interferon type I (IFN-I) in these diseases is not fully understood.

Purpose of the Study:

  • To investigate the expression of the IFN-I-associated MxA protein in patients with PMR and TA.
  • To determine if MxA protein expression differs between PMR patients, controls, and TA patients.

Main Methods:

  • Immunocytochemistry was used to screen temporal artery biopsies for MxA protein and other markers (CD83, CD68, CD3, S100).
  • Non-inflamed biopsies from 11 PMR patients and 13 controls were compared.
  • Inflamed biopsies from 4 TA patients were also analyzed.

Main Results:

  • Focal MxA expression was observed in non-inflamed arteries, occurring more frequently in PMR patients than in controls.
  • MxA expression was more prevalent in adventitial dendritic cells (DCs) in PMR patients.
  • Activated adventitial DCs were identified in PMR patients, but MxA expression in TA biopsies was not spatially linked to inflammation.

Conclusions:

  • MxA protein expression in PMR and TA patient arteries indicates that IFN-I influences both non-inflamed and inflamed vessel walls.
  • Further research is needed to clarify IFN-I's potential role in the initiation of PMR and TA.
  • IFN-I may act as a bridge between innate and adaptive immunity in these autoimmune disorders.

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