IL-23 ELISA Kit, Mouse

It has been reported that IL-12 has potent antitumor activity in a variety of murine tumor models, causing regression of established tumors and inhibiting the formation of experimental metastases and spontaneous metastases. On the other hand, it has recently been reported that genetic deletion or antibody-mediated elimination of IL-23 in mice leads to increased infiltration of cytotoxic T cells into the transformed tissue, rendering a protective effect against chemically-induced carcinogenesis. So far, it has been reported that expression of IL-23 and its receptors is detectable in activated macrophages, DCs, and keratinocytes in healthy skin. It was also demonstrated that the human oral squamous cell carcinoma (HOSCC) cell line, HSC-3, spontaneously expresses IL-23 and its receptors mRNA and protein. IL-23 up-regulates the growth and cell proliferation of oral cancer by promoting the nuclear transactivation of RelA.² Human IL23 has been shown to stimulate the production of IFN-gamma by PHA blast T-cells and memory T-cells. It also induces proliferation of both cell types. Human monocyte-derive macrophages produce IL23 in response to virus infection (Sendai virus but not Influenza A virus). Expression of p19 in transgenic mice leads to runting, systemic inflammation, infertility, and death before 3 months of age. The animals show high serum concentrations of the pro-inflammatory cytokines TNF-alpha and IL1. The number of circulating neutrophils is increased. Acute phase proteins are expressed constitutively. It was also shown that IL23 plays a prominent role in the regulation of granulopoiesis and the prevalence of neutrophil-regulatory T-cells.³