In:
Drug Development Research, Wiley, Vol. 75, No. S1 ( 2014-11)
Abstract:
Postmarketing Phase IV Tumor necrosis factor alpha ( TNF ‐α) is a pleiotropic cytokine that plays a central role in the immune system functioning and in the pathogenesis of rheumatoid arthritis ( RA ). TNF ‐α inhibition has been demonstrated effective to treat RA ; however, response to anti‐ TNF ‐α therapies is heterogeneous, with roughly one‐third of patients not achieving disease control. Identification of a biological marker to assess the effectiveness of TNF‐α inhibition may help to discriminate patients with a reduced response to anti‐TNF‐α agents. The aim of this study was to assess whether anti‐ TNF ‐α treatment was able to modify the cytokine network interfering with interferon gamma ( INF γ) release after phytohemagglutinin ( PHA ) stimulation of peripheral blood mononuclear cells ( PBMCs ) from RA patients, according to disease activity. We found that RA patients with active disease had low release of INF γ after PHA stimulation, but anti‐ TNF ‐α agents were able to modify INF γ production. In anti‐ TNF ‐α responders, we observed a higher release of INF γ, achieving levels comparable with those seen in healthy subjects. The ability of PBMCs from RA patients to release INF γ may serve as a biomarker of disease activity and response to anti‐ TNF ‐α. Larger studies are needed to validate these data.
Type of Medium:
Online Resource
ISSN:
0272-4391
,
1098-2299
DOI:
10.1002/ddr.2014.75.issue-s1
Language:
English
Publisher:
Wiley
Publication Date:
2014
detail.hit.zdb_id:
1500191-X
SSG:
15,3
