**Background**
Interleukin-12 (IL-12) is a critical pro-inflammatory cytokine that plays a pivotal role in the regulation of the immune response, particularly in the induction of Th1 cell differentiation and the production of interferon-gamma (IFN-γ). The p40 subunit is a shared component of both IL-12 and IL-23, making it a strategic target for modulating inflammatory pathways. Dysregulation of IL-12 signaling is implicated in various autoimmune and metabolic disorders, including rheumatoid arthritis, multiple sclerosis, and type 1 diabetes. Consequently, neutralizing the p40 subunit provides a powerful tool for investigating the mechanisms of immune-mediated tissue destruction and developing therapeutic interventions. In this context, we will introduce an inhibitor of the p40 subunit – Anti-Mouse IL-12 p40 Antibody.
**Definition**
Anti-Mouse IL-12 p40 Antibody (C17.8) is a rat-derived IgG2a κ type monoclonal antibody that specifically binds to the p40 subunit of mouse IL-12 to inhibit its biological activity.
**In Vitro and In Vivo Studies**
According to the Anti-Mouse IL-12 p40 Antibody description, this antibody framework is stable and specific, allowing it to bind both antigens and endogenous immune receptors. In terms of Anti-Mouse IL-12 p40 Antibody in vitro application, it is suitable for p40 affinity chromatography, immunoprecipitation, ELISA, and flow cytometry. Extensive Anti-Mouse IL-12 p40 Antibody in vivo studies have demonstrated its potent inhibitory effects across multiple disease models. In non-obese diabetic (NOD) mice, administration of 500 μg (i.p., twice weekly from 5-30 weeks) completely prevented diabetes and significantly decreased the degree of insulitis. Conversely, administration of 200 μg (i.p., for 6 consecutive days) to 2-week-old NOD mice resulted in the inhibition of IL-2 and IFN-γ at 4 weeks, but subsequently enhanced their production at 8 weeks, leading to a rapid onset of overt diabetes. In models of streptococcal cell wall (SCW)-induced arthritis, a dose of 0.5 mg (i.p., 2 hours before SCW injection) suppressed arthritis by increasing chondrocyte PG synthesis, reducing synovial membrane inflammatory cell infiltration, and decreasing mRNA levels of IL-1β, IL-12, and TNFα. Furthermore, 0.5 mg (i.p., once weekly) significantly prolonged survival in myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis mice. In conclusion, Anti-Mouse IL-12 p40 Antibody is a highly effective tool for neutralizing IL-12 p40 in the study of autoimmune and inflammatory pathologies.
Keywords
Anti-Mouse IL-12 p40 Antibody (C17.8), Interleukin Related, IL, IL-12, P40, Inflammation, Immunology, Diabetes, Arthritis, Inhibitor, inhibitor, inhibit
References
[1] Fujihira K, et al. Suppression and acceleration of autoimmune diabetes by neutralization of endogenous interleukin-12 in NOD mice. Diabetes. 2000 Dec;49(12):1998-2006.
[2] Joosten LA, et al. Blockade of endogenous interleukin 12 results in suppression of murine streptococcal cell wall arthritis by enhancement of interleukin 10 and interleukin 1Ra. Ann Rheum Dis. 2000 Mar;59(3):196-205.
[3] Gaignage M, et al. Novel antibodies that selectively block mouse IL-12 enable the re-evaluation of the role of IL-12 in immune protection and pathology. Eur J Immunol. 2021 Jun;51(6):1482-1493.