The Sjl/j T Cell Response to Both Spontaneous and Transplantable Syngeneic Reticulum

The Reticulum Cell Sarcoma (RCS)' is a spontaneous lymphatic tumor of the SJL/J (H-29) mouse, first observed by Murphy (1) in upwards of 90% of SJL/J mice of amean age of 13 .3 mo. RCS tumors are considered B cell lineage neoplasms that exhibit Ig H chain gene rearrangements, but no surface or cytoplasmic Ig (2). Additionally, RCS tumors express IAs MHC-encoded polypeptides (3) . RCS tumors require an obligate syngeneic host CD4+ T cell response for growth (4, 5) . The in vivo passive administration of Gk1.5 mAb (anti-CD4) or haplotype-specific anti-Ia antibody to SJL/J mice, before or shortly after transfer of the transplantable RCS line, RCS LA-12, resulted in the complete abrogation of tumor growth (5, 6) . The nature of the RCS tumor-associated antigen responsible for the stimulation of syngeneic T cell proliferation has remained elusive . However, Katz et al . (7) made the observation that both the in vivo growth of RCS and the in vitro RCS-specific T cell response correlated with the lack of IE expression . Studies by Wilbur et al . (8, 9) further implicated the role of IE in tumor growth . Furthermore, two of four RCS-specific T cell hybridomas when cocultured with IEdor IEk-bearing allogeneic spleen cells were stimulated to release T cell growth factors, such as IL-2 (10) . Recently, Kappler et al . (11) have developed an mAb, termed KJ23a, which specifically interacts with TCR containing the V0 17a variable segment gene products . Interestingly, only mice that lack thymic IE exhibit KJ23a+ T cells in the periphery, since V017a expression confers IE reactivity and are deleted by IE-expressing mice (12) . SJL/J (IE) mice possess KJ23a+ T cells in their periphery. Since the RCS tumors stimulate T cells that appear to recognize "IE-like" antigens and IE+ Fl mice failed to support RCS tumor growth, we undertook studies to examine the role that V(317a+ (KJ23a+ ) T cells may play in the RCS-specific T cell response .