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Genetic control of cell-mediated lympholysis to trinitrophenyl (TNP)-modified murine syngeneic cells. Expression of Ir gene function at the cytotoxic precursor and helper cell

Journal Article · · J. Immunol.; (United States)
OSTI ID:5677519
The present study investigates some of the cellular mechanisms responsible for the defect in cytotoxic T lymphocyte (CTL) response to trinitrophenyl (TNP)-modified H-2/sup b/ self components in C57Bl/6(H-2/sup b/) or (C57BL/6 x C3H/He)(H-2/sup b/ x H-2/sup k/)F/sub 1/ mice. C3H/He, C57BL/6, and (C57BL/6 x C3H/He)F/sub 1/ mice were immunized to TNP-modified self by skin painting with trinitrochlorobenzene, and their spleen cells were used a) for in vitro secondary sensitization to syngeneic spleen cells conjugated with limiting concentrations of trinitrobenzene sulfonate (TNP-self) or b) as a source of radioresistant helper cells for augmenting the TNP-self CTL response generated by spleen cells from unimmunized C3H/He, C57Bl/6, and F/sub 1/ mice. The results indicate that strong or weak in vitro secondary CTL responses could be obtained in the H-2/sup k/ or H-2/sup b/ strain, respectively. This strain-dependent genetic difference was also observed in (H-2/sup b/ x H-2/sup k/)F/sub 1/ mice. These results permit the detection of the Ir gene defect in the anti-TNP-H-2/sup b/ self CTL response at both the helper and cytotoxic precursor cell levels.
Research Organization:
National Institutes of Health, Bethesda, MD
OSTI ID:
5677519
Journal Information:
J. Immunol.; (United States), Journal Name: J. Immunol.; (United States) Vol. 126:3; ISSN JOIMA
Country of Publication:
United States
Language:
English