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The Journal of Immunology, Vol 150, Issue 12 5519-5528, Copyright © 1993 by American Association of Immunologists
ARTICLES |
VK Tsiagbe, J Asakawa, A Miranda, RM Sutherland, Y Paterson and GJ Thorbecke
Department of Pathology, New York University School of Medicine, New York 10016.
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 gamma-irradiated syngeneic hosts. A superantigen-like stimulation by RCS cells was borne out by the fact that all the RCS-specific hybridomas used V beta 16 in their TCR. RCS cells did not stimulate I-As-restricted, V beta 17a+ KLH- specific, or V beta 1+ heme-specific hybridomas, but were excellent Ag presents for these cells. Preincubation of RCS cells with high concentrations of the KM core peptide (high affinity for I-As) did not interfere with the ability of RCS to stimulate RCS-specific hybridomas. The relative representation of mRNA for V beta 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 V beta 16 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 V beta 16 in mRNA, but not of V beta 17a mRNA.
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