RGD Reference Report - Increased IL-17A expression in temporal artery lesions is a predictor of sustained response to glucocorticoid treatment in patients with giant-cell arteritis. - Rat Genome Database

RGD Reference Report - Increased IL-17A expression in temporal artery lesions is a predictor of sustained response to glucocorticoid treatment in patients with giant-cell arteritis. - Rat Genome Database

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Increased IL-17A expression in temporal artery lesions is a predictor of sustained response to glucocorticoid treatment in patients with giant-cell arteritis.
Authors:	Espigol-Frigole, G Corbera-Bellalta, M Planas-Rigol, E Lozano, E Segarra, M Garcia-Martinez, A Prieto-Gonzalez, S Hernandez-Rodriguez, J Grau, JM Rahman, MU Cid, MC
Citation:	Espigol-Frigole G, etal., Ann Rheum Dis. 2013 Sep 1;72(9):1481-7. doi: 10.1136/annrheumdis-2012-201836. Epub 2012 Sep 19.
RGD ID:	8698666
Pubmed:	PMID:22993227 (View Abstract at PubMed)
DOI:	DOI:10.1136/annrheumdis-2012-201836 (Journal Full-text)
BACKGROUND: Interleukin 17A (IL-17A) exerts pivotal proinflammatory functions in chronic inflammatory and autoimmune diseases. OBJECTIVE: To investigate IL-17A expression in temporal artery lesions from patients with giant-cell arteritis (GCA), and its relationship with disease outcome. METHODS: Fifty-seven patients with biopsy-proven GCA were prospectively evaluated, treated and followed for 4.5 years (52-464 weeks). Relapses, time (weeks) required to achieve a maintenance prednisone dose <10 mg/day, and time (weeks) to complete prednisone withdrawal were prospectively recorded. IL-17A mRNA was measured by real-time quantitative RT-PCR in temporal arteries from all patients and 19 controls. IL-17 protein expression was assessed by immunohistochemistry/immunofluorescence. RESULTS: IL-17A expression was significantly increased in temporal artery samples from GCA patients compared with controls (6.22+/-8.61 vs 2.50+/-3.9 relative units, p=0.016). Surprisingly, patients with strong IL-17A expression tended to experience less relapses, and required significantly shorter treatment periods (median 25 vs 44 weeks to achieve <10 mg prednisone/day, p=0.0079). There was no correlation between IL-17A and RORc or RORalpha expression suggesting that these transcription factors may not exclusively reflect Th17 differentiation, and that cells other than Th17 cells might contribute to IL-17 expression in active patients. Accordingly, FoxP3(+)IL-17A(+) cells were identified in lesions by confocal microscopy and were dramatically reduced in specimens from treated patients. CONCLUSIONS: IL-17A expression is increased in GCA lesions, and is a predictor of response to glucocorticoid treatment. The contribution of FoxP3+ cells to IL-17A production in untreated patients suggests that induced-Tregs may facilitate disease remission when proinflammatory cytokine production is downregulated by glucocorticosteroids.

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Object Symbol	Species	Term	Qualifier	Evidence	With	Notes	Source	Original Reference(s)
IL17A	Human	temporal arteritis	severity	IEP		mRNA and protein:increased expression:temporal artery (human)	RGD
Il17a	Rat	temporal arteritis	severity	ISO	IL17A (Homo sapiens)	mRNA and protein:increased expression:temporal artery (human)	RGD
Il17a	Mouse	temporal arteritis	severity	ISO	IL17A (Homo sapiens)	mRNA and protein:increased expression:temporal artery (human)	RGD

Genes (Rattus norvegicus)


Il17a (interleukin 17A)

Genes (Mus musculus)


Il17a (interleukin 17A)

Genes (Homo sapiens)


IL17A (interleukin 17A)