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Compared with the mixed leukocyte reaction (MLR) between cells from healthy individuals, the MLR between cells from two patients with multiple sclerosis (MS) is, on average, reduced in strength. There is a tendency for the most marked reduction of MLR to occur when both or neither of the members in a tested pair carry HL-A7, and when cells from patients in a relatively early stage of the disease (short duration, relapses but no permanent disablement) are studied; especially when cells from these patients are used as reactor clels in the MLR. Repeated studies of the same cell combinations with varying intervals showed that when both members of the pair carry HL-A7,--and therefore have a large chance also to carry LD-7a--the MLR strength is relatively constant. When only one or neither of the members carry HL-A7, the strength of MLR varies considerably. Probably two different mechanisms exist in MLR impairment: similarity of LD genes, and "immunosuppressive" factors which can vary during the course of the disease.

Three healthy HLA-B7 homozygous subjects were found with similar but not identical HLA-D antigens; one was DW 2 homozygous according to independent typing results. This could be an expression of `long' and `short' HLA-.D antigens or be due to differences in weak antigens outside the HLA-D region. Two further healthy HLA-.B7 homozygous subjects were studied; one was apparently heterozygous for DW 2, the other apparently carried no DW 2 antigen. Both could discriminate between different DW 2 homozygous test cells. Two such test cells-one from a patient with multiple sclerosis (MS) and the other from a man with two children with MS-gave variable and absurd reactions with cells from the two subjects in question. It is tentatively suggested that genes exist which, when present in both moities in a mixed leucocyte reaction (MLR), can impair the MLR and give false `typing' reactions. This might be more common among patients with MS and perhaps also some other diseases (certain arthritides, e.g. rheumatoid arthritis) than among healthy subjects and can complicate or make impossible the interpretation of HLA-.D typing data. It could also explain the previously-described impaired MLR between cells from patients with these diseases. [ABSTRACT FROM AUTHOR]