EZ Cap™ Mouse IL-10 mRNA (m1Ψ)

Interleukin-10 (IL-10) is an important anti-inflammatory cytokine that is mainly secreted by immune cells such as T cells, B cells, monocytes and macrophages. IL-10 helps maintain the balance of the immune system by inhibiting the production and release of pro-inflammatory cytokines, which can inhibit the activation of macrophages and dendritic cells and reduce their ability to present antigens, thereby reducing the strength of the immune response. In addition, IL-10 also promotes the proliferation of B cells and the production of antibodies, which has a positive effect on humoral immunity. Because of its powerful immunomodulatory function, IL-10 has received much attention in the study of autoimmune diseases, inflammatory diseases, and transplant rejection. Studies have shown that the lack or abnormal function of IL-10 may lead to the development of chronic inflammation and autoimmune diseases. IL-10 is therefore considered a potential therapeutic target for the development of novel anti-inflammatory drugs and immunomodulatory therapies.

EZ Cap™ Mouse IL-10 mRNA (m1Ψ) is provided at a concentration of ~1 mg/ml with Cap1 structure. There are currently two ways to cap mRNA: One is co-transcription method, by adding Cap analogues into the transcription process. The other is enzymatic Capping. After transcription, Cap0 capping is performed by Vaccinia virus Capping Enzyme (VCE), GTP and S-adenosylmethionine (SAM). The Cap0 is then generated into the Cap1 through 2´-O-Methyltransferase and SAM. Cap1 Capping can also be performed by adding VCE, 2´-O-Methyltransferase, GTP and SAM in a one-step process. Cap 1 structure is more ideal for mammalian systems and possess higher transcription efficiency than Cap 0 structure. The addition of N1-Methylpseudo-UTP(m1Ψ) and poly(A) tail suppress RNA-mediated innate immune activation and increase the stability and lifetime of the mRNA in vitro and in vivo. Poly(A) tail also plays an important role in enhancing the efficiency of translation initiation.