When the immune system is triggered by an infectious agent histiocytes (macrophages and dendritic cells), NK-cells, and cytotoxic T-lymphocytes
(CTLs) are activated, mutually stimulating each other via receptor interaction, as well as secretion of a variety of inflammatory cytokines and chemokines.
As with survivin overexpression (5-7), livin overexpression by cancer cells may lead to anti-livin antibody responses and cytotoxic T-lymphocyte
responses against the cancer.
According to pre-clinical results, these PME-CD40L dendritic cells drive stronger effector memory in cytotoxic T-lymphocytes
(CTLs) in comparison to mature dendritic cells generated with cytokines alone, making them better able to recognize cancer antigens.
The telomerase-specific cytotoxic T-lymphocytes
(CTLs) isolated from the peripheral blood of vaccinated study subjects killed telomerase targets in vitro.
The authors had previously found that telomere loss in cytotoxic T-lymphocytes
(CTLs), the cells responsible for killing HIV-infected cells, was accelerated in AIDS patients, and contributed to the loss of anti-HIV activity that occurs during disease progression.
Those publications, as well as subsequent research, demonstrated that messenger RNA encoding the catalytic reverse transcriptase protein component of human telomerase (hTERT mRNA), when introduced into dendritic cells, can stimulate the immune system to produce cytotoxic T-lymphocytes
(CTLs, or killer T-cells) capable of recognizing and destroying telomerase-positive cancer cells.
Telomerase was introduced into human dendritic cells by gene transfer enabling the dendritic cells to generate telomerase specific cytotoxic T-lymphocytes
(CTLs) that killed all three tumor cell lines.