Despite much effort, the structural features of the surface molecules responsible for antigen recognition by thymus-derived (T) cells remain unclear (l, 2) . Progress in this area will in part depend on the availability of homogeneous T cells from which to isolate and purify T cell receptor molecules in quantities sufficient to characterize them. With the advent of recent technology, the development ofT cell clones (3), and the description of mitogen-induced T cell growth factors (TCGF; 4, 5), t it has become possible to generate and maintain clones of antigen-specific T cells indefinitely in culture in appreciable numbers .In this communication, we provide a preliminary characterization of long-termcultured lines and clones of cytotoxic T lymphocytes (Tc) with specificity directed to determinants of the Igh-l b immunoglobulin (Ig) allotype . These cell lines and clones were initiated by repeated stimulation of Igh-l ó-immune BALB/c spleen cells with an Igh-l b -producing myeloma (6), and subsequent maintenance in vitro in medium supplemented with mitogen-induced growth factors.These cloned allotype-specific Tc are unique in that their cytotoxic activity can be inhibited by soluble antigen, i.e., Igh-l b . In view of the available extensive knowledge of the Igh-l b molecule, the antigen in this system, it seems likely that these allotypespecific Tc will prove to be useful starting material for both detailed studies of killer T cell functions and for molecular characterization of their receptors .Volume 154 August 1981 491-500

We show that determinants of IgG(2a) of C57BL/6 mice (Igh-1(b)) stimulate allotypespecific T cells in BALB/c mice. Such cells are detected in two different functional assays; chronic allotype suppression and T cell-mediated cytotoxicity. A population of suppressor T cells capable of inducing chronic Igh-1(b) suppression was demonstrated by rosetting procedures to possess Igh-1(b)-specific receptors, a result interpreted as indicating that suppressor T cells may act directly upon allotype-bearing B cells. From similar populations we were also able to demonstrate Igh-1(b)-specific cytotoxic T cells. Such cells were lytic for target myeloma cells expressing the Igh-1(b) allotype of IgG28, and were ineffective against a variant cell line failing to express Igh-1(b), and other target cell lines expressing different allotypes or isotypes. The similar specificity of suppressor T cells and cytotoxic T lymphocytes for Igh-1(b) allotype raises the possibility that the target in allotype suppression is a B cell, and that allotype-specific cytotoxic T cells may play some role in regulation of allotype expression in the suppressed state.

The lineage of natural killer (NK) cells is poorly understood. To examine the relationship between NK cells and cells of the T lineage we have examined purified NK cells from a mutant mouse strain (scid) with severe combined immunodeficiency. Approximately 40% of the lymphoid cells in the spleens of scid mice expressed the NK-specific marker NK-2.1. All NK activity of the scid spleen cells could be accounted for by the NK-2.1+ population, similar to results obtained by using normal C57BL/6 X DBA/2 (B6D2F1) mice. Sorted NK-2.1+ cells proliferated in response to human recombinant interleukin 2 (r-IL 2) but not to concanavalin A (Con A), and were maintained in culture for 2 to 3 wk. Cultured NK-2.1+ cells displayed a cell surface phenotype (Asialo-GM1+, Thy-1.2+, L3T4-, Lyt-2-) and lytic activity similar to that described for freshly isolated NK cells of normal mice. Furthermore, T cell receptor (TCR) genes of the TCR-gamma and TCR-beta loci were in germline configuration, and no functional transcripts of TCR-gamma, TCR-beta, or TCR-alpha were detected. We propose that the expression of the TCR is not necessary for functional NK activity, and NK cells are distinct from both mature cytotoxic T lymphocytes and the earliest identifiable T cells.