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Ulcerative colitis is a disease of widely varying severity. The course in any patient is difficult to predict. In this community repeated episodes commonly lead to a chronic active stage, in which the sufferer becomes an invalid unless the process is relieved by colectomy. In this phase exacerbations and com plications are common, and not infrequently lead to death. It is with patients in this group that the present trial has been concerned. While ulcerative colitis as representative of an autoimmune disorder fails to fill all the criteria enumerated by McKay and Burnet (1963) for autoimmune disease, there remains strong evidence for immunological disturbance. This evidence has been reviewed by Kirsner (1961). I do not propose to discuss at length whether this disturbance represents a normal response to modified tissue or a defect of the immune mechanism. I consider the action of antimetabolites, together with observa tions made during this therapy, supports the view of primary tissue damage or modification. With the exception of steroid hormones, the most powerful suppressants of the immune response, as measured by failure of graft rejection, are all agents developed for the treatment of cancer. These agents may be considered in their main groupings?nitrogen mustard and its derivatives, the sulphur mustards, the antimetabolites, and antibiotics. There is prob ably some selectivity of action of these agents, antagonism occurring between the antimetabolites, mercaptopurine, and the folic-acid antagonists. In our early trials we used the anti metabolites mercaptopurine and 6-thioguanine. More recently the sulphur mustard busulphan has been employed.

RECENT extirpation studies from several laboratories have indicated that the thymus may play a major role in immune reactions. In rabbits thymectomized at birth, there is suggestive evidence that humoral antibody production is impaired.’ Rats thymectomized shortly after birth have a diminished capacity to make antibody against and to develop Arthus sensitivity to bovine serum albumin (BSA )#{149}2 Thymectomy of adult rabbits, however, appears not to affect ability to make antibody.3’5 Guinea pigs thymectomized as adults have been reported to show a slight impairment of antibody formation.#{176} The response of the thymectomizedanimal is also impaired in a variety of delayed hypersensitive reactions. Miller,7 Martinez et al.8 and we#{176}’1#{176} have shown that skin homograft rejection is markedly delayed in animals thymectomized shortly after birth. Rats thymectomized within a week of birth have a compromised capacity todevelop both tuberculin sensitivity and delayed reactivity against BSA-a pure protein antigen.2” The thymectomized rat is incapable of developing experimental allergic encephalomyelitis, an autoimmune disease thought to be mediated by delayed hypersensitivity.9” Adjuvant induced rat arthritis, however, appears to be uninfluenced by thymectomy.� The histologic concomitant of this gross immunologic incompetence is a specific depletion of small lymphocytes from blood, spleen and lymph nodes.7’9’11’12 In contrast, at least in the rat, germinal centers, plasma cells, and reticuloendothelial elements (blood monocytes, Kupifer cells, microglia of nervous tissue, reticulum cells of splenic red pulp ) are unaltered by thymectomy, and plasma protein values, including y-globulin, are normal by paper electrophoresis.2’12 Miller has shown that replacement with intact viable thymus restores homograft reactive capacity in the mouse.7 Injection of thymic homogenates, in contrast, does not restore immunologic competence to the thymectomized rat.2 Thymectomy of older animals has generally failed to influence antibody production46 or delayed reactions2’7’8’� although rats thymectomized as late as 3 weeks after birth have shown a decreased delayed reactive capacity against protein antigens.2 It is possible that early thymectomy is necessary to produce immunologic incompetence. This situation is perhaps analagous to that in chickens undergoing surgical removal of the bursa of Fabricius. The bursa, a lymphoid structure strikingly similar to the thymus, arises as an out

Summary.— This paper deals with the pathogenesis and the microscopic and cytological features of the pemphigus group of diseases. The immunological aspects of acantholysis are discussed. The statement by several authors that pemphigus is an autoimmune disease is questioned and evidence from the literature against this hypothesis is cited.

A .\L 0 :11 G the current concepts regarding mechanisms through which autoimmune diseases may develop is the thesis that neoplastic tissues may he so altered that the usual self-recognition mechanisms break down and the body may produce antibodies against the neoplastic cells which ('an then react against the host's own cells." This paper reports the finding of Hashimoto's thyroiditis, considered an autoimmune disease, in a benign cystic teratoma.