Nature 270, 522 - 524 (08 December 1977); doi:10.1038/270522a0

Absence of suppressor cells from rats bearing passively enhanced kidney allografts

J. R. BATCHELOR^†, L. BRENT^‡ & P. J. KILSHAW^*‡

^†McIndoe Research Unit, Queen Victoria Hospital, East Grinstead, Sussex, UK
^‡Department of Immunology, St Mary's Hospital Medical School, London W2, UK
^*Present address: Nutrition Department, National Institute for Research in Dairying, Shinfield, Reading, Berkshire, UK.

LYMPHOCYTES which inhibit the immunological responses of other lymphocytes are known as suppressor cells, and such cells have been shown to mediate both specific and nonspecific unresponsiveness in many experimental situations¹⁻³. In the context of allotransplantation, Kilshaw et al. ^4,5 have found that the highly strain-specific unresponsiveness to skin allografts induced in adult mice by pretreatment with donor strain tissue extract and Bordetella pertussis vaccine, followed by a short post-operative course of antilymphocyte serum (ALS), is at least in part mediated by thymus-dependent lymphocytes. Thus, transfer of 25−100 10⁶ spleen cells (optimally the lower dose⁵) from mice in the stable phase of unresponsiveness into ALS-treated syngeneic recipients established a long-lasting unresponsiveness to donor strain skin grafts in up to 50% of recipients. Because the nature of the mechanisms of immunological enhancement of kidney allografts in rats remain unclear⁶⁻⁸ we have carried out cell transfer experiments similar to those of Kilshaw et al. in order to discover whether suppressor cells also play a part in mediating the stable phase of the enhanced state. Fabre and Morris⁹ have previously failed to transfer unresponsiveness with spleen cells from rats with enhanced kidneys, but it is possible that transfer of cells to normal, syngeneic rats—as in their experiments—is an insufficiently sensitive method for detecting suppressor cells. Our results show that it is unlikely that suppressor cells or auto-anti-idiotype antibodies are responsible for the steady state of enhancement. A more likely explanation involves the induction of unresponsiveness by the continuous exposure of the recipient to histocompatibility antigens in the absence of Ia-like antigens—the latter determinants being obligatory requirements for the activation of T cells 'helping' both potentially reactive B cells and T cells capable of differentiating into killer cells.

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