Scandinavian journal of rheumatology · 2009
Expression of the class I interferon-related MxA protein in temporal arteries in polymyalgia rheumatica and temporal arteritis.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Nordborg C, Larsson K, Aman P, Nordborg E
Аннотация
OBJECTIVE: The aim of this study was to assess the expression of the interferon type I (IFN-I)-associated MxA protein in polymyalgia rheumatica (PMR) and temporal arteritis (TA).
METHODS: Non-inflamed temporal artery biopsies from 11 PMR patients were compared with biopsies from 13 patients given other diagnoses. Coded sections were screened immunocytochemically for MxA protein, CD83, CD68, CD3, and S100 protein. Inflamed temporal artery biopsies from four patients with TA were also investigated.
RESULTS: Focal MxA expression was seen in non-inflamed arteries, more frequently in PMR than in controls (p = 0.0124). MxA expression was also more common in adventitial dendritic cells (DCs) in PMR (p = 0.0124). Activated adventitial DCs were detected in PMR. Focal MxA expression in the inflamed biopsies from the patients with TA was not related spatially to the inflammation.
CONCLUSIONS: The expression of MxA protein in arteries from patients with PMR and TA shows that non-inflamed and inflamed vessel walls are influenced by IFN-I. Further studies are required to elucidate whether IFN-I plays a role in the initiation of PMR and/or TA, serving as a link between the innate and the adaptive immune responses, as in some other autoimmune disorders.
METHODS: Non-inflamed temporal artery biopsies from 11 PMR patients were compared with biopsies from 13 patients given other diagnoses. Coded sections were screened immunocytochemically for MxA protein, CD83, CD68, CD3, and S100 protein. Inflamed temporal artery biopsies from four patients with TA were also investigated.
RESULTS: Focal MxA expression was seen in non-inflamed arteries, more frequently in PMR than in controls (p = 0.0124). MxA expression was also more common in adventitial dendritic cells (DCs) in PMR (p = 0.0124). Activated adventitial DCs were detected in PMR. Focal MxA expression in the inflamed biopsies from the patients with TA was not related spatially to the inflammation.
CONCLUSIONS: The expression of MxA protein in arteries from patients with PMR and TA shows that non-inflamed and inflamed vessel walls are influenced by IFN-I. Further studies are required to elucidate whether IFN-I plays a role in the initiation of PMR and/or TA, serving as a link between the innate and the adaptive immune responses, as in some other autoimmune disorders.