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May 1966


Author Affiliations

University of Leeds The General Infirmary Leeds, 1

Arch Dermatol. 1966;93(5):637-638. doi:10.1001/archderm.1966.01600230141044

To the Editor:  We were greatly interested in Dr. Nurse's theory of the cause of psoriasis, described in your February 1966 correspondence section because we1 have recently arrived at diametrically-opposite conclusions. Dr. Nurse attributes the hyperplasia of the epidermis in psoriatic lesions to a deficiency in a mitotic inhibitor, whereas we infer that the abnormality is caused by the emergence of a mutant mitogenic effector.Following Swann,2 we postulate3 that symmetrical mitosis in the cells of an organized tissue is normally inhibited as the result of the specific contact relations that exist between cells of a similar differentiation. Mitotic inhibition should depend upon the London-van der Waal's self-recognition forces that operate between identical tissue coding factors (TCF) on contiguous cytoplasmic membranes.3 TCF includes histocompatibility antigens. In normal growth, this mitotic inhibition has to be overcome by a specific mitogenic effector, two broad classes of which can

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