Syngeneic Response to SJL Follicular Center B Cell Lymphoma (Reticular Cell Sarcoma) Cells Is Primarily in Vβ16⁺ CD4⁺ T Cells

The growth of SJL B cell lymphomas (RCS, reticulum cell sarcoma) in vivo and in vitro is known to depend on cytokine production by RCS-responsive host CD4⁺ T cells. The high frequency of RCS responsive cells in normal SJL lymph nodes prompted us to prepare a set of 21 RCS-specific T cell hybridomas. Like normal SJL T cells, these hybridoma cells respond to RCS, but not to normal syngeneic B cells; produce IL-2, IL-4, and IL-5; and promote growth of RCS in γ-irradiated syngeneic hosts. A superantigen-like stimulation by RCS cells was borne out by the fact that all the RCS-specific hybridomas used Vβ16 in their TCR. RCS cells did not stimulate I-A^s-restricted, Vβ17a⁺ KLH-specific, or Vβ1⁺ heme-specific hybridomas, but were excellent Ag presenters for these cells. Preincubation of RCS cells with high concentrations of the KM core peptide (high affinity for I-A^S) did not interfere with the ability of RCS to stimulate RCS-specific hybridomas. The relative representation of mRNA for Vβ 1, 4, 10, 15, 16, and 17a was evaluated in RNA extracted from normal SJL lymph node cells responding to Con A or to RCS cells. Only Vβ16 was specifically enriched in the response to RCS. Moreover, the degree of responsiveness to RCS cells in lymph node cells from F₁ hybrids of SJL and I-E transgenic SJL mice, corresponds to the relative abundance of Vβ16 in mRNA, but not of Vβ17a mRNA.