RESUMO
Objective To explore the antigen presentation of CT26.WT via intra-peritoneal injection. Methods The intra-peritoneal injection model was made via injecting cell suspensions in mice. The spleen was isolated from BALB/c mice toco-culture with CT26.WT to detect tumor-killed ability. Phenotype identification methods and CCK8 massy were used to measure the ability of antigen presentation and stimulate T lymphocyte proliferation. IHC was used to detect the expression of B7H4 in normal and tumor tissues. Results Along with the extension of intra-peritoneal injection, the surviving number of cells was increased, contrary to the apoptosis. DC cells failed in maturation and impaired in stimulating T lymphocyte proliferation. B7H4 was higher in tumor tissues. Conclusions With the extension of intra-peritoneal injection, the mature DC cells were scared in number, resulting in the impairement of antigen-presentation. Moreover, the higher B7H4 expression in tumor tissues led to the lack of second signals which may stimulate T cells. Consequently, the ability of T cells in killing tumor cells was decreased so that they escape immunosurveillance.
RESUMO
In the present experiment, we investigated the im munoprophylactic and immunotherapeutic effects of transferring spleen LAK cells or " LAK-88/DC " cells from 615 inbred mice against mouse leukemia. The results showed that transferring LAK cells or "LAK-88/DC" cells and injecting conditional medium for a week 21 days before L615 inoculation induced significant prophylactic effects, which cured 80% of the L615-sufferring mice. Injecting conditional medium alone was also effective, which cured 60% of the mice, While transferring LAK cells or "LAK-88/DC" cells at the same time with L615 inoculation or 1 day after L615 inoculation presented no apparent therapeutic effect. However, when combined with cyclophosphamide (CY) chemotherapy, the transfer of LAK cells or "LAK-88/DC " cells 5 days after L615 inoculation could prolong the mean survival time and even cured 25%-28.6% of the advanced L615 leukemic mice.