Key result
Arid5a deficiency inhibits IL-6 elevation and suppresses TH17 cell development in mice.
Why the study?
Posttranscriptional regulation of IL-6 mRNA stability beyond Regnase-1 was largely uncharacterized, motivating investigation of Arid5a's role.
Population
Macrophages and LPS-treated mice and experimental autoimmune encephalomyelitis mouse models
Comparison
Arid5a deficiency vs normal Arid5a function
Design
Preclinical experimental study
Authors
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Arid5a inhibition may blunt IL-6-driven inflammation in models; leaves open translation to human autoimmune disease.
Arid5a is a unique RNA binding protein that stabilizes IL-6 mRNA, promoting inflammatory processes and autoimmune diseases.
Masuda et al. (2013) studied Experimental autoimmune encephalomyelitis. Arid5a deficiency was evaluated on IL-6 serum level and development of T(H)17 cells. Arid5a deficiency inhibited the elevation of IL-6 serum levels in LPS-treated mice and suppressed IL-6 levels and T(H)17 cell development in experimental autoimmune encephalomyelitis.
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