AI Article Synopsis
- IL-1β is a proinflammatory molecule that plays a key role in both innate and adaptive immune responses, and it significantly contributes to autoimmune arthritis by enhancing the bone-resorbing ability of regulatory T cells (Tregs).
- Research using mice lacking the IL-1 receptor antagonist showed that blocking IL-1β was more effective in reducing early arthritis symptoms and bone damage than treating established cases.
- The study found that Tregs in inflamed joints had altered behavior, producing RANKL, which promotes bone erosion, and similar T cells were identified in human rheumatoid arthritis, linking IL-1β activity to joint damage.
Article Abstract
IL-1β is a proinflammatory mediator with roles in innate and adaptive immunity. Here we show that IL-1β contributes to autoimmune arthritis by inducing osteoclastogenic capacity in Tregs. Using mice with joint inflammation arising through deficiency of the IL-1 receptor antagonist (Il1rn-/-), we observed that IL-1β blockade attenuated disease more effectively in early arthritis than in established arthritis, especially with respect to bone erosion. Protection was accompanied by a reduction in synovial CD4+Foxp3+ Tregs that displayed preserved suppressive capacity and aerobic metabolism but aberrant expression of RANKL and a striking capacity to drive RANKL-dependent osteoclast differentiation. Both Il1rn-/- Tregs and wild-type Tregs differentiated with IL-1β accelerated bone erosion upon adoptive transfer. Human Tregs exhibited analogous differentiation, and corresponding RANKLhiFoxp3+ T cells could be identified in rheumatoid arthritis synovial tissue. Together, these findings identify IL-1β-induced osteoclastogenic Tregs as a contributor to bone erosion in arthritis.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8439607 | PMC |
| http://dx.doi.org/10.1172/JCI141008 | DOI Listing |
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