IL-23/Th17 axis is not influenced by TNF-blocking agents in ankylosing spondylitis patients.

Autor: Milanez FM; Division of Rheumatology, Faculdade de Medicina da Universidade de São Paulo - Reumatologia, Av. Dr. Arnaldo, n° 455, 3° andar, sala 3192, São Paulo, SP, 05403-010, Brazil. femanente@terra.com.br., Saad CG; Division of Rheumatology, Faculdade de Medicina da Universidade de São Paulo - Reumatologia, Av. Dr. Arnaldo, n° 455, 3° andar, sala 3192, São Paulo, SP, 05403-010, Brazil. goncalves-carla@uol.com.br., Viana VT; Division of Rheumatology, Faculdade de Medicina da Universidade de São Paulo - Reumatologia, Av. Dr. Arnaldo, n° 455, 3° andar, sala 3192, São Paulo, SP, 05403-010, Brazil. visatv@gmail.com., Moraes JC; Division of Rheumatology, Faculdade de Medicina da Universidade de São Paulo - Reumatologia, Av. Dr. Arnaldo, n° 455, 3° andar, sala 3192, São Paulo, SP, 05403-010, Brazil. juliocbmoraes@yahoo.com.br., Périco GV; URC - Unidade Radiológica Criciúma, Rua Antonio de Lucca, 139 - Centro - Criciúma, Santa Catarina, SC, 88811-503, Brazil. gregoryperico@hotmail.com., Sampaio-Barros PD; Division of Rheumatology, Faculdade de Medicina da Universidade de São Paulo - Reumatologia, Av. Dr. Arnaldo, n° 455, 3° andar, sala 3192, São Paulo, SP, 05403-010, Brazil. pdsampaiobarros@uol.com.br., Goncalves CR; Division of Rheumatology, Faculdade de Medicina da Universidade de São Paulo - Reumatologia, Av. Dr. Arnaldo, n° 455, 3° andar, sala 3192, São Paulo, SP, 05403-010, Brazil. goncalves.reuma@uol.com.br., Bonfá E; Division of Rheumatology, Faculdade de Medicina da Universidade de São Paulo - Reumatologia, Av. Dr. Arnaldo, n° 455, 3° andar, sala 3192, São Paulo, SP, 05403-010, Brazil. eloisa.bonfa@hc.fm.usp.br.
Jazyk: angličtina
Zdroj: Arthritis research & therapy [Arthritis Res Ther] 2016 Feb 24; Vol. 18, pp. 52. Date of Electronic Publication: 2016 Feb 24.
DOI: 10.1186/s13075-016-0949-6
Abstrakt: Background: Advances in pathophysiology and treatment of ankylosing spondylitis (AS) was recently demonstrated. However, the effect of anti-TNF in the newly described inflammatory pathways involved pathogenesis of this disease remains to be determined. The aim of our study was, therefore, to investigate long-term influence of anti-TNF drugs in IL-23/IL-17 axis of AS patients and their possible correlation with treatment, clinical, laboratory and radiographic parameters.
Methods: Eighty-six AS anti-TNF naïve patients, 47 referred for anti-TNF therapy (active-AS; BASDAI ≥ 4) and 39 with BASDAI < 4 (control-AS) were included. The active group was evaluated at baseline, 12-months and 24-months after TNF blockade and compared at baseline to control-AS group and to 47 healthy age- and gender-matched controls. Plasma levels of IL-17A, IL-22, IL-23 and PGE2 were measured. Non-steroidal anti-inflammatory drugs (NSAIDs) intake were recorded every 6 months. Radiographic severity and progression was assessed by mSASSS at baseline and 24 months after therapy.
Results: At baseline, active-AS group presented higher IL-23 and PGE2 levels compared to control-AS group (p < 0.001 and p = 0.008) and to healthy controls (p < 0.001 and p = 0.02). After 24-months of TNF blockade, IL-23 and PGE2 remained elevated with higher levels compared with the healthy group (p < 0.001 and p = 0.03) in spite of significant improvements in all clinical/inflammatory parameters (p < 0.001). Further analysis of 27 anti-TNF-treated patients who achieved a good response (ASDAS-CRP < 2.1,with a drop ≥ 1.1) at 24-months revealed that IL-23 plasma levels remained higher than healthy controls (p < 0.001) and higher than control-AS group with similar disease activity (ASDAS-CRP < 2.1, p = 0.01). In active-AS group (n = 47), there was a strong correlation between IL-23 and IL-17A at baseline, 12-months and 24-months after anti-TNF therapy (p ≤ 0.001).
Conclusion: This study provides novel data demonstrating that the IL-23/IL-17 axis is not influenced by TNF blockade in AS patients despite clinical and inflammation improvements and NSAID intake.
Databáze: MEDLINE
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