Final answer:
Activated IELs, particularly CTLs, mediate enterocyte apoptosis when their TCRs detect antigens presented by MHC I molecules, leading to the release of perforin and granzymes that induce a controlled cell death, or apoptosis. This mechanism is augmented by the fas ligand pathway and supported by the secretion of cytokines like interferons which enhance immune recognition.
Step-by-step explanation:
Activated intraepithelial lymphocytes (IELs), which encompass activated cytotoxic T cells (CTLs), mediate enterocyte apoptosis primarily through the release of perforin and granzymes upon recognition of infected or abnormal cells. These CTLs detect cells presenting MHC I-embedded antigens, such as those of virally infected cells, through their T-cell receptors (TCRs). When an IEL's TCR binds to an antigen presented by MHC I, it signals the activation of the CTL.
Following activation, the CTL releases perforin and granzymes, which work synergistically to induce apoptosis. Perforin forms pores in the target cell membrane, facilitating the entry of granzymes, which are proteases that trigger the apoptotic pathway within the infected cell. This leads to orderly cell death, preventing the spread of the infection and protecting surrounding tissues. Additionally, CTLs can induce apoptosis through the fas ligand pathway, where the fas ligand on the CTL binds to the fas molecule on the target cell, again leading to programmed cell death.
Moreover, CTLs and NK cells have complementary functions in the immune response, and can release cytokines such as interferons that help other immune cells recognize and eliminate infected cells, and prevent the release of viral particles.