Lack of suppressive effect of α-foetoprotein on development of experimental allergic encephalomyelitis in rats

Abstract

α-FOETOPROTEIN (AFP) is a major glycoprotein that occurs in substantial amounts in mammalian sera and body fluids during foetal and early neonatal life. Unusually high levels of AFP have been observed in the amniotic fluid in association with congenital abnormalities of the central nervous system (CNS)^1,2. Abnormal amounts have also been found in adults with hepatic and gastrointestinal malignancy^3,4. AFP has attracted attention as a potential immunoregulatory protein with suppressive activity for immune responses of mammalian lymphoid cells^5–7, including autosensitisation. For example, normal rat serum prevents adult rat lymphoid cells from reacting immunologically to self-antigens in vitro⁸. In rats with experimental allergic encephalomyelitis (EAE), a prototypic autoimmune disease of the CNS⁹, a serum factor has been reported which causes suppression of proliferative responses of rat lymphoid cells exposed to mitogens¹⁰. Peak serum suppressive activity paralleled increasing α-globulin concentration and coincided with reversal of disease. We have reported¹¹ that development of EAE is impaired in suckling rats of an age when high levels of AFP would be expected. Using two rat model systems, we have dissociated AFP production, assessed by serum concentration, from the occurrence of EAE. Our findings suggest that AFP does not have a major suppressive role in the development of this autoimmune disease.