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• W2073289045 abstract "It is proposed that the sex and age distributions of SLE, together with other evidence, are consistent with the following conclusions: (1) The disease has a disturbed tolerance autoimmune etiology and is restricted to a particular subpopulation characterized by a specific genotype. (2) Probably three dominant X-linked alleles feature in the SLE genotype, together with autosomal factors at one or more (perhaps two) loci. The X-linked factors account for the sex ratio of carriers. (3) Phenotypic initiation of SLE in a carrier depends upon the accumulation of three independent random events. (4) The average rate of each of these events is more or less constant from birth to the end of the life span, although the rate of each event in females is twice the corresponding rate in males. (5) These random events are probably some form of somatic mutation of X-linked genes in stem cells of the lymphoid series. (6) If each of the three somatic mutations affects a different gene—and this is probable although not certain—then the three mutations may generate genetically nonidentical but independent forbidden clones. (7) There is an interval or latent period between the occurrence of the last somatic mutation and the onset of SLE. In female infants this average interval is about one and a half years, but in adolescent and adult females it is about five years. In adult males it is, perhaps, about two and a half years, although better statistics are needed to confirm this. (8) During this latent period, the proliferation of forbidden clones of lymphocytes carrying cell-bound autoantibodies is presumed to occur and cytological damage to target tissues accumulates; there is an endogeneous defense mechanism—acting partly in the thymus and involving plasma cells and humoral antibody—directed against autoantigenic forbidden clones; on the average, this mechanism is more efficient in females than in males. (9) The endogeneous defense mechanism is vulnerable to various extrinsic factors such as certain drugs, infections and stress. (10) The pattern of organ involvement should partly depend upon the genotype of the patient and the distribution of “tissue coding factors” (in the target organs) that are complementary to the cellbound autoantibodies. (11) Antinuclear antibodies and lupus erythematosus cells are the consequences rather than the causes of SLE." @default.
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• W2073289045 title "Systemic lupus erythematosus" @default.
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• W2073289045 doi "https://doi.org/10.1016/0002-9343(65)90199-3" @default.
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