Effector cells capable of mediating lysis

With reproducible methods of generating effector cell populations and assessing target cell death, thy-mus-derived (T) lymphocytes were identified as the principal effector cells involved in antigen-specific CML. T lymphocytes have been divided functionally into helper T lymphocytes (TH) or cytolytic T lymphocytes (CTLs) based on the apparent predominant function of these cells. However, recent studies indicate that there is considerable functional overlap among these populations. The capacity to demonstrate the lytic potential of a given lymphocyte population depends in part on the nature of the target cells used. Other T cell populations, whose recognition mechanisms are less well characterized than those of CD4+ TH and CD8+ CTL, are also capable of mediating lysis. These include the CD4/CD8 double negative a(3 TCR-positive T cells and the yƓ TCR-positive T cells.

Lymphoid cells other than T lymphocytes can also display lytic activity against certain target cells. Natural killer (NK) cells are lymphoid cells that have the capacity to lyse certain transformed target cells such as K562 (human) or YAC-1 (murine) by a process that does not involve MHC restriction. NK activity occurs in cells having the morphology of large granular lymphocytes (LGLs); these cells express distinctive cell surface markers but they are not well defined with respect to their lineage. Natural killer lysis involves events similar to those that have been identified in antigen-specific lysis by CTLs, and may involve similar mechanisms. NK cells bear receptors for the Fc portion of immunoglobulin G (IgG); these receptors allow NK cells to lyse antibody-coated target cells by a process referred to as antibody-dependent cellular cytotoxicity (ADCC). Cells having properties that are distinguishable from those of NK cells and CTLs, termed killer (K) cells, also function as effector cells in ADCC. Finally, lytic activity can be induced in lymphoid cells in culture by exposure to supraoptimal concentrations of interleukin 2 (IL-2), which leads to the induction of lymphokine-activated killer (LAK) cells.

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