High impact information on IL18

• CONCLUSION: This study demonstrated that in situ in OA cartilage, the stimulation of chondrocytes by NO is at least partly responsible for the up-regulation of ICE and IL-18 synthesis while decreasing the level of the ICE inhibitor PI-9 [1].
• The coding sequence for dog IL-18 was obtained using reverse transcription-polymerase chain reaction from mRNA harvested from PMA-stimulated alveolar macrophages [2].
• In particular, we measured the amount of parasites in samples such as blood, lymph nodes and skin, and the expression levels of IFN-gamma, IL-2, IL-4, IL-10, IL-12 and IL-18 cytokines in the blood [3].
• At all levels of the respiratory mucosa, the most abundant transcripts were those encoding IL-18 and TGF-beta [4].
• The results obtained from freshly isolated PBMC showed expressions of TNF-alpha, IL-2, IFN-gamma, IL-10 and IL-18 mRNA, similar to those from non-infected dogs [5].

Analytical, diagnostic and therapeutic context of IL18

• Based upon sequence analysis, we propose that this new gene is the dog equivalent of human IL-18 [2].
• At 12 weeks after surgery, cartilage from the femoral condyles and tibial plateaus were processed for immunohistochemistry for ICE, IL-18, and protease inhibitor 9 (PI-9), a natural inhibitor of ICE, followed by morphometric analysis [1].

References