MODIFICATION OF BIOLOGIC RESPONSE IN EXPERIMENTAL HYPERSENSITIVITY

Recently there has been wider acceptance of the view that a particular group of diseases and certain reactions to therapeutic agents occur on the basis of an acquired hypersensitivity. There is evidence that rheumatic fever, glomerulonephritis, serum sickness and periarteritis nodosa belong in this category,¹ and some have added to this group acute disseminated lupus erythematosus and scleroderma.²

The lesions of acute glomerulonephritis and rheumatic fever generally occur after a definite interval following infection, and lesions resembling periarteritis nodosa have appeared after an interval following the administration of certain drugs or a foreign serum.³ It has generally been accepted that the development of host hypersensitiveness during this interval is the essential pathogenetic basis for the subsequent morphologic alterations characteristic of these diseases and that the lesions observed result from the union of the responsible antigen with its antibody in the tissues of the sensitized host. The contention