ANIMALS deficient in lymphoreticular function either by age, genotype or immunosuppression are more susceptible to infection by most known pathogens mainly on account of their depressed immunological responses. An intact lymphoreticular system (LRS), however, can itself contribute to disease by various mechanisms including; providing sites for multiplication¹, producing infectious complexes² and precipitating autoaggressive accompaniments and sequalae³. It is possible that a special class of this paradoxical relationship is exemplified by the slow encephalopathies of which the best understood is scrapie, others being kuru, Creutzfeldt-Jakob disease and mink encaphalopathy. In these diseases of the central nervous system, infection normally occurs by some peripheral route and there always seems to be an initial, probably obligatory, replicative phase in the LRS before gaining access to the target organ^4,5. In spite of this involvement of the LRS, and indicating some very special relationship as its basis, there is a complete absence of conventional immunological responses. No scrapie-specific antibodies⁶ or interferons⁷ have been found, and this is not due to any generalised depression of immune reactions⁸. Immunosuppressive techniques, which severely impair the functions of the B and T-cell elements of the LRS, do not affect the pathogenesis of peripherally injected scrapie^9,10. Also congruent with an absence of immune responses is the non-inflammatory nature of the brain lesions even in the later stages of the disease^11,12.