Anti-IL21 (aa 24-152) polyclonal antibody

In a Wistar rat model, prolonged supplementation of mustard seed (MS) to the diet significantly ameliorates the induction of colorectal carcinomas by 1,2-dimethylhydrazine (DMH). The expression of the splenocyte major histocompatibility complex class I (MHCI) was found significantly enhanced, whereas that of the major histocompatibility complex class II (MHCII) was significantly decreased. Compared to that of control animals, the proportion of spleenic B- and dendritic cells (DC) was amplified in the MS group. The expressions of MHCI, as well as that of MHCII, were increased in DC cells; whereas in B cells, MHCI expression was augmented but that of MHCII moderately decreased. The percentages of CD8+CD28+ and CD4+CD28+ cells were increased in the MS group, while the CD4+CD25+Foxp3+ subset was depressed. Plasma analysis showed that DMH-exposure induced amplified amounts of interleukin (IL)-4, IL-5, IL-10, and transforming growth factor-beta, whereas MS feeding counteracted this effect but enhanced IL-2,IL12p70,IL21, TNF-alpha, and interferon-gamma. In the SW480 colon adenocarcinoma cell-line, the cytotoxicity of spleenic T-cells from MS-fed animals was significantly increased. In the DMH-exposed rats, the expression of perforin in the spleenic T-cells was dramatically decreased, whereas MS abolished this depression. In summary, dietary MS suppresses DMH-induced immuno-imbalance as well as colon carcinogenesis in rats.

T cell-mediated cell immunity is the main antitumor immunity in which the effector T cells need specific antigen and costimulatory signals. One of the vaccines applied in tumor immunotherapy is the gene-modified tumor cell vaccine. One potential method to increase cell epitope density is to link the antigen with the major histcompatibility complex subunit beta 2m. Our previous research indicated that the strategy of epitope fusion gene OVA-linker-beta 2m can promote the formation of specific compounds on the tumor cell surface in vitro. In this study, we constructed two coexpression vectors pGL3-CD80-OVA-linker-beta 2m and pGL3-IL21-OVA-linker-beta 2m, in order to explore the cooperative action of CD80 or interleukin-21 (IL21) with the epitope fusion gene in anti-tumor immunity. Results showed that gene-modified B16 cells (B16/OVA, B16/CD80-OVA and B16/IL21-OVA) grew slower than B 16 cells in vitro and in vivo, especially the B16/IL21-OVA subline, which illustrated that such gene modification decreased oncogenicity of malignant tumor cells. On the other hand, gene-modified tumor cell subline immunization can induce effective long-term anti-tumor immunity defending tumor cell attacks. IL21 played a more cooperative role with the OVA-linker-beta 2m than CD80 in this study. This strategy might lay foundations for the research of a new type of tumor vaccine.