Zentralblatt für Bakteriologie, Parasitenkunde, Infektionskrankheiten und Hygiene 232 [antikvár]

Zbl. Bakt. Hyg., I. Abt. Orig. A 232, 1-7 (1975) Aus der Bayerischen Landesimpfanstalt Münclien (Leiter : Professor Dr. H. Stickl) und dem Max-Planck-Institut für Psychiatrie, München (Leiter: Professor Dr. G.Peters) Sensibilisierung gegen Antigene des Zentralnervensystems nach experimenteller Infektion mit Vaccinia-Virus I. Nachweis einer zellulären Sensibilisierung^ Sensitization Against the Antigens of the Brain after Experimental Vaccinia Infection I. Evidence for Cell-Mediated Immune Response to Brain-Antigens H.Chr. Huber, K.H. zinn, V. Hochstein-Mintzel, j. Simon und H. Stickl Eingegangen am 26. Oktober 1974 Abstract Vaccinia virus infection was performed by scarification of the shaved skin (5X5 cm-) on the back of Pirbright guinea pigs. The macrophage migration inhibition test was performed with peritonealexudate cells 7, 11, 14 and 21 days after infection. Macrophage migration inhibition occured after exposure of the cells to whole brain tissue antigen on the 7">, 11"', 14day after infection (s. table 1). Lymphocyte transformation responses were examined by i''C-2-Thymidin uptake using blood cultures and basic encephalitogenic protein and whole brain tissue extract as antigens. A positiv transformation response could be demonstrated from one to 8 weeks after infection (s. table 2). The specifity of the transformation response to brain antigen was established using control cultures stimulated with PHA or PPD. In no case stimulation occured with PPD. Stimulation with PHA was not altered. On the other hand the spontaneous lymphocyte transformation was enhanced at one week after infection and lymphocyte cultures exposed to heat inactivated vaccinia virus showed transformation from the 3 week after infection until the end of the observation period (i.e. 8 weeks) (s. table 2). The reason why cell mediated hypersensitivity to brain antigen is induced following vaccinia infection remains unknown. The most probable among several possible mechanisms seem a) the induction of virus-specific antigens on the surface of infected cells or b) the release of brain specific antigen through virus infection. ^ Mit Unterstützung der Deutschen Forschungsgesellschaft. 1 Zbl Bakt. Hyg., I. Abt. Orig. A 232