Barish M E, Raissdana S S
Department of Physiology and Biophysics, California College of Medicine, University of California, Irvine 92717.
Brain Res. 1990 Mar 5;510(2):329-34. doi: 10.1016/0006-8993(90)91385-t.
We have investigated the capacity of the lymphokine gamma-interferon (IFN-gamma) to induce class II major histocompatibility complex (MHC) antigens on astrocytes cultured from BALB/c mice. This is a mouse strain resistant to experimental allergic encephalomyelitis (EAE), and in a recent report Massa et al. (Proc. Natl. Acad. Sci. U.S.A., 84 (1987) 4219-4223) indicated that BALB/c astrocytes in vitro were not susceptible to class II MHC antigen induction by IFN-gamma. We observed, in agreement with this previous report, that when primary cultures of astrocytes from neonatal BALB/c mice were just at confluence (7-10 days in vitro), IFN-gamma did not stimulate expression of class II MHC antigens. However, after 14-16 days in vitro, a population of astrocytes emerged in the cultures on which class II MHC antigens could be induced. These cells expressed the astrocyte marker glial fibrillary acidic protein, and were found in close association to small round superficial cells (multipotential precursor cells), and to microglia. These results indicate that the ability of astrocytes to respond to lymphokine stimulation is not completely correlated with susceptibility to EAE, and further suggest the importance of central mechanisms in the development of inflammatory brain disease.