Cationic liposomes bearing IL-2 on their external surface induced mice leukocytes to kill human cervical cancer cells in vitro, and significantly reduced tumor burden in immunodepressed mice.

Tumor cells are known to modify their surroundings in order to escape immunologic detection, and IL-2, a killer cell activator, is one of the factors known to overcome this escape mechanism. In this regard, when we cocultured cells from the human cervical cancer cell line INBL with mice blood leukocytes, no inhibition of tumor cell growth was observed, but when a similar coculture was done in the presence of cationic liposomes bearing IL-2 on their external surface (CL-IL-2), all the INBL cells were killed. In order to evaluate whether this in vitro property of CL-IL-2 to overcome tumor cell detection by lymphocytes could also be reproduced in vivo, INBL cells were intraperitoneally (i.

Evidence that cervical cancer cells secrete IL-2, which becomes an autocrine growth factor.

We present evidence that cervical cancer cells express a functional IL-2 receptor (IL-2R). In fact, by RT-PCR we obtained that the IL-2R is present in CALO, and INBL cells, and that it consisted of the alphaIL-2R, betaIL-2R, and gammaIL-2R chains. We also found that IL-2 is a growth factor for these cell lines, and unexpectedly that CALO and INBL themselves being cancer cells produce, and secrete IL-2.

Characterization of cationic liposomes having IL-2 expressed on their external surface, and their affinity to cervical cancer cells expressing the IL-2 receptor.

Anionic, cationic, and neutral liposomes were constructed to contain IL-2 in order to evaluate their affinity to a cervical cancer cell line (INBL) and to determine whether they can present IL-2 on their external surface. When these liposomes were co-cultured with INBL, the anionic liposomes were the only ones found to be cytotoxic. When neutral and cationic liposomes were constructed in the presence of IL-2, IL-2 was detected only on the surface of cationic liposomes by using a fluorescent anti-IL-2 antibody.