CTL Cell

Cytotoxic T lymphocyte (CTL) cells, also known as CD8+ T cells, are immune cells that destroy any cell thought to be a threat to the integrity of the host, from virally infected cells to spontaneous tumors.1 CTLs offer protection against intracellular pathogens by killing the infected cell before the pathogens can proliferate and further infect the neighboring cells.2

Activation of naïve CTLs to effector cells is required prior to these cells exerting their cytotoxic potential.2 CTLs comprise a distinct lymphocyte class that responds to various stimuli such as major histocompatibility antigens, protein antigens, viruses, as well as intracellular bacteria and parasites. These cells recognize peptides bound to the MHC class I molecules, and exposure to specific antigens results in the activation and proliferation of CTLs. Activated CTLs secrete cytolytic mediators (eg, perforin) and also cause target cell apoptosis.3 CTLs kill the target cells via cell-cell interactions or secretion of cytokines (IFN-γ and TNF-α).1 Cytokine secretion enhances antigen presentation and mediation of antipathogenic effects.3 CTL reorganizes its cytoskeleton to focus its killing apparatus on the target cell and avoids killing neighboring cells by secreting its toxic proteins into a confined space.2

CTLs perform an important function of destroying intracellular pathogens or cancer cells, and disease control can be achieved by modulation of CTL production or activation.3 Derangements in CTLs result in autoimmune diseases (including autoimmune skin disorders), neoplastic disease, and possibly allergic contact dermatitis.1

​APC: antigen-presenting cell; CD: cluster of differentiation; IFN-γ: interferon gamma; MHC: major histocompatibility complex; TNF: tumor necrosis factor.

References:

  • 1.

    Andersen MH, Schrama D, Thor Straten P, Becker JC. J Invest Dermatol. 2006;126:32-41.

  • 2.

    Alberts B, Johnson A, Lewis J, Raff M, Roberts K, Walter P. Molecular Biology of the Cell, 4th edition. New York: Garland Science. 2002.

  • 3.

    Ito H, Seishima M. J Biomed Biotechnol. 2010;2010:641757.