Pediatr Res 2002 Aug;52(2):175-179
Ohlenbusch A, Pohl D, Hanefeld F.
Abteilung Padiatrie, Schwerpunkt Neuropadiatrie, Georg-August-Universitat, 37075 Gottingen, Germany.
Myelin oligodendrocyte glycoprotein (MOG) is a quantitatively minor glycoprotein of the CNS localized preferentially on the outermost myelin lamellae and the oligodendrocyte plasma membrane.
In several animal models, MOG displays highly immunogenic properties by inducing a severe multiple sclerosis-like disease, characterized by inflammatory demyelinating lesions.
Immunologic findings implicate MOG as a target autoantigen in multiple sclerosis.
We have performed a molecular study on the MOG gene by sequencing the promotor and the entire coding region, as well as the exon-intron boundaries, in 75 children with multiple sclerosis.
A total of five unknown polymorphic sites in the promotor region not affecting any of the putative cis-acting transcriptional regulation motifs as well as nine additional base changes in four different exons each with similar distribution in patients and controls (n = 100) were detected.
Exon 2 coding for the Ig-like domain revealed two rare heterozygous missense mutations, possibly altering favorable conformational epitopes (P43H; R66P).
P43 is part of the encephalitogenic epitope MOG(35-55).
A putative C1q binding site in the C"-D loop of the Ig superfamily motif encompasses R66.
In conclusion, the polymorphisms observed do not provide evidence to support a significant role for MOG in multiple sclerosis susceptibility.