In situ Ia expression on brain cells in the rat: autoimmune encephalomyelitis-resistant strain (BN) and susceptible strain (Lewis) compared

Abstract

In order to examine in situ Ia expression on brain cells of various strains of rat, experimental autoimmune encephalomyelitis (EAE) was induced in both EAE-susceptible (LEW) and EAE-resistant (BN) strains. For induction of EAE in the resistant strain, two methods were applied: one was injection of guinea-pig myelin basic protein (GPBP) in complete Freund's adjuvant into LBNF1----BN chimeras; the other was transfer of GPBP-reactive T-line cells from BN rats into syngeneic rats. LBNF----BN chimeras developed clinical EAE, whereas BN rats that received T-line cells did not. However, histological EAE was apparent in both groups. Immunohistochemical examination using two different monoclonal antibodies (OX3 and OX6) against rat Ia antigens revealed that microglia of LEW, BN and chimera rats expressed Ia antigens in the central nervous system (CNS) with EAE. On the other hand, astrocytes were negative for Ia antigens in all the strains. Furthermore, quantitative analysis was undertaken in order to compare the density of Ia-positive microglia in the BN CNS with that in the LEW CNS. It was revealed that the density of Ia-positive microglia in the vicinity of perivascular inflammatory cell aggregates was essentially the same in both strains regardless of the difference in methods of EAE induction or histological severity of the disease. Ia-positive microglia remote from inflammatory cell aggregates were somewhat fewer in rats with mild histological EAE. However, no strain difference was noted in this analysis. Therefore, we concluded that in situ Ia-inducibility on the brain cells of EAE-resistant rats is not different from that of EAE-susceptible rats. Although Ia-positive microglia in both strains may be involved in the immune responses in the CNS, it is unlikely that the difference in Ia-inducibility on brain cells would contribute to strain-specific susceptibility to EAE.