Tag

Interleukin 10

All articles tagged with #interleukin 10

IL-10 Autoantibodies May Drive Inflammatory Bowel Disease in a Subset of Patients
science19 days ago

IL-10 Autoantibodies May Drive Inflammatory Bowel Disease in a Subset of Patients

A 2026 NEJM study analyzing data from more than 4,900 people with inflammatory bowel disease found that about 3.5% carry autoantibodies that block interleukin-10, effectively removing an anti-inflammatory brake and potentially driving disease in this subset; the autoantibibody presence is linked to the HLA-DRB1*01:03 variant, suggesting possibilities for early genetic testing and more targeted, mechanism-based therapies.

Immune signals and hormones may explain why women's pain lingers longer
health4 months ago

Immune signals and hormones may explain why women's pain lingers longer

New research combining mouse experiments with human vehicle‑crash data suggests that pain after injury lasts longer in women because monocytes produce less IL-10, a molecule that both reduces inflammation and directly dampens pain signals; testosterone boosts IL-10 production in male monocytes, helping men recover faster. This shifts the view of the immune system from solely driving pain to also helping resolve it, pointing to therapies that enhance the body's natural pain‑resolution pathways to prevent chronic pain.

Immune signals and testosterone may explain why women's pain lasts longer
health4 months ago

Immune signals and testosterone may explain why women's pain lasts longer

A new Science Immunology study of 245 people with traumatic injuries, plus mouse experiments, suggests women’s pain lasts longer because their immune system is less effective at shutting off pain; men have higher interleukin-10, and testosterone boosts interleukin-10 production, helping pain fade faster. The findings, which align with observed sex differences in chronic pain, could guide future treatments (including hormone-based options) while acknowledging that pain biology is not explained by a single pathway.