Immunosuppressive activities of rat antisera raised against supernates from skin-graft-primed cells
Rat antisera raised against supernates derived from draining lymph node cells of skin-graft-primed mice exhibit a number of immunosuppressive effects in vitro and in vivo. The skin graft-induced, cell-free-supernates had been demonstrated to contain a number of helper activities that led to an antig...
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Veröffentlicht in: | Transplantation 1985-10, Vol.40 (4), p.405-412 |
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Sprache: | eng |
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Zusammenfassung: | Rat antisera raised against supernates derived from draining lymph node cells of skin-graft-primed mice exhibit a number of immunosuppressive effects in vitro and in vivo. The skin graft-induced, cell-free-supernates had been demonstrated to contain a number of helper activities that led to an antigen-specific induction of cytolytic T lymphocytes and/or to the induction of interleukin-2 synthesis. The rat antisera administered to skin graft recipients resulted in prolongation of major-histocompatibility-complex-incompatible skin graft survival. The rat antisera appear to have a specificity for the inhibition of T cell responses in vitro, although binding to B and T cells was apparent. The responses of unprimed cells to T cell mitogens and alloantigens are blocked, whereas B cell responses to the lipopolysaccharide mitogen are not blocked by the antisera. The generation of cytolytic T lymphocytes and the cytolytic functions of such cells are both blocked by the rat antisera. The inhibition of the differentiation pathway in cells cultured continuously with the antisera was overcome only through the addition of conditioned medium obtained from stimulated concanavalin A rat spleen cells, as opposed to mouse cell conditioned media. The rat antisera do not appear to block T cell responses via the IL-2 receptor, and were found to be substantially less effective against activated and proliferating T cells. These rat antisera have allowed us to further examine the pathways involved in T cell responses. |
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ISSN: | 0041-1337 1534-6080 |
DOI: | 10.1097/00007890-198510000-00012 |