Interleukin-35 as a key immunoregulatory mediator in steroid-hyporesponsive severe asthma - PubMed
4 hours ago
- #immunoregulation
- #asthma
- #steroid-resistance
- Severe asthma remains a major clinical challenge due to corticosteroid hyporesponsiveness in some patients.
- Steroid hyporesponsiveness is linked to impaired glucocorticoid receptor signaling, MAPK/NF-κB activation, and HDAC2 dysfunction.
- Regulatory immune networks, including regulatory T and B cells, are compromised in severe asthma.
- Current biologics (anti-IgE, anti-IL-5/IL-5Rα, anti-IL-4Rα) have limited efficacy in steroid-hyporesponsive asthma.
- IL-35 emerges as a key immunoregulatory cytokine, suppressing inflammation and restoring corticosteroid sensitivity.
- IL-35 inhibits Th17-driven inflammation, MAPK/NF-κB signaling, and expands regulatory immune networks.
- Potential therapeutic target for steroid-hyporesponsive severe asthma by addressing immune dysregulation and steroid resistance.