SYNGENEIC RESPONSE TO SJL FOLLICULAR CENTER B-CELL LYMPHOMA (RETICULAR CELL-SARCOMA) CELLS IS PRIMARILY IN V-BETA-16-CELLS( CD4+ T)

The growth of SJL B cell lymphomas (RCS, reticulum cell sarcoma) in vi vo and in vitro is known to depend on cytokine production by RCS-respo nsive 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-specifi c T cell hybridomas. Like normal SJL T cells, these hybridoma cells re spond to RCS, but not to normal syngeneic B cells; produce IL-2, IL-4, and IL-5; and promote growth of RCS in gamma-irradiated syngeneic hos ts. A superantigen-like stimulation by RCS cells was borne out by the fact that all the RCS-specific hybridomas used Vbeta16 in their TCR. R CS cells did not stimulate I-A(s)-restricted, Vbeta17a+ KLH-specific, or Vbeta1+ heme-specific hybridomas, but were excellent Ag presenters for these cells. Preincubation of RCS cells with high concentrations o f the KM core peptide (high affinity for I-A(s)) did not interfere wit h the ability of RCS to stimulate RCS-specific hybridomas. The relativ e representation of mRNA for Vbeta 1, 4, 10, 15, 16, and 17a was evalu ated in RNA extracted from normal SJL lymph node cells responding to C on A or to RCS cells. Only Vbeta16 was specifically enriched in the re sponse 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, c orresponds to the relative abundance of Vbeta16 in mRNA, but not of Vb eta17a mRNA.