SUMMARY Gm allotypes were detected and quantitated by radioimmunoassay (RIA) in paired serum and CSF samples from patients suffering from various neurological diseases. Of 115 patients with neurological disorders (65 MS and 50 others), seven subjects displayed one or two allotypes in their CSF which were absent in serum. The Gm phenotype in the patient's serum allowed us to infer the genotype without the need of familial data. A comparison of the regression curves obtained in RIA from the unexpected allotype in CSF and the counterpart in a normal serum pool argued for an identity of the Gm antigen carried by both inhibitory molecules. The unexpected allotype(s) in CSF can be considered as the product of a latent Gm gene which may be activated by either immune perturbations due to the disease per se or some particular immune regulations in the central nervous system.

The major histocompatibility complex (MHC) is a system of closely linked genes showing an extremely high degree of polymorphism. These genes are major elements in the government of specific immune reactions. Consequently they may represent a genetic marker system well suited to investigate variability in selective pressure from disease agents on different populations. On this background we have started investigation of the MHC complex in reindeer (Rangifer tarandus L). The MHC complex consist of polymorphic regions as well as regions conserved during evolution which should allow the use of crossspecies reagents. We have shown that human MHC gene probes hybridize with genomic DNA from reindeer, and thus can be used as a tool in reindeer MHC research. By RFLP (restriction fragment length polymorphism) analysis using these probes we have also been able to show polymorphism in MHC related genes from reindeer.

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