["Particular neutralizing monoclonal antibodies to certain cytokines act as agonists in vivo by protection of the cytokine's active site and prolongation of cytokine half-life. While this principle might be useful for targeted immunotherapy, its role in the pathogenesis of inflammation and autoimmunity is unclear.", "We sought to determine whether slight, structurally non-relevant modifications of the prototypic pro-inflammatory cytokine interleukin-1β (IL-1β) during an immune response could elicit polyclonal anti-IL-1β antibody responses that modulated IL-1β's in vivo activity.", 'We engineered two different IL-1β variants, thereby mimicking the process of cytokine modification occurring during inflammation, and conjugated them to virus-like particles, followed by immunization of mice. The resulting polyclonal anti-IL-1β antibody responses were assessed using in vitro and in vivo assays as well as two relevant (auto-) inflammatory murine models.', 'While antibody responses generated to one variant were potently inhibiting IL-1β, antibody responses induced by the other variant even potentiated the in vivo effects of IL-1β; the latter led to enhanced morbidity in two different IL-1β-mediated mouse models, including a model of inflammatory bowel disease and an inflammatory arthritis model.'] Do endogenous polyclonal anti-IL-1 antibody responses potentiate IL-1 activity during pathogenic inflammation?