Basophilic cells in scrapings and pieces of nasal mucosa removed from the inferior turbinates of adult patients with house dust nasal allergy, and pieces of oral mucosa from normal subjects were examined electronmicroscopically. Three distinct types of basophilic cells were identified; blood basophil leukocytes (predominantly in the subepithelium), mucosal mast cells (predominantly in the epithelium), and connective tissue mast cells (similar to the oral connective tissue mast cells and predominantly in the deeper lamina propria). The mucosal mast cells were closer in morphology to the basophil leukocytes than to the connective tissue mast cells.

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A case of interstitial cystitis was encountered, which we believe to have been caused by an allergy to shrimp and squid. The 33-year-ord male patient, who had been suffering from incurable bladder irritability since 1965, first visited our clinic in 1975. His past history and the sampling of shrimp and squid led us to suspect that they could be responsible for his condition. The provocation tests was done by injection of the extract into the hypodermis and vesical cavity. This led to a recurrence of symptoms similar to the chief complaints and, at the same time, increased the levels of histamine and serotonin in the blood and urine. Omitting shrimp and squid from the diet has prevented a recurrence of the symptoms.

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Antigen-induced morphological changes of basophils were studied in atopic asthmatics sensitive to house dust, using phase-contrast microscopic motion pictures. 1. There was no significant difference in random movement of basophils from healthy and asthmatic subjects before addition of antigen. Before the addition of antigen incidence of oriented movement of basophils taken from atopic asthmatics was lower than that of basophils from healthy subjects. 2. Sensitized basophils, characterized by a low incidence of oriented movement, were clearly activated and showed oriented movement upon stimulation with antigen. 3. The incidence of oriented movement by active basophils increased significantly at 6-9 min and peaked at 12-15 min after addition of antigen. 4. Degranulation of basophils started to occur at 3-6 min and peaked at 12-15 min following addition of antigen.

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Low temperature-dependent activation of complement system, also called cold activation of complement, was studied. The whole hemolytic complement (CH50) in sera from four cases which had revealed the above phenomenon was markedly reduced while that of plasma taken in the presence of EDTA was within normal range. As for the complement components, reduced levels of C4, C1INH, C3 and C9 were observed, while Clq, Cls, B, P, H and I were at normal levels. The cause of such marked reduction of C4 in those patients was discussed in terms of its synthesis and its role in activation of the complement system. Although repeated analysis of sera taken from patients with cold activation of complement revealed the reduced level of complement, hereditary factors were discarded as an explanation of reduced complement titer.

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When mouse spleen or bone marrow cells were cultured in the presence of medium conditioned by concanavalin A-stimulated splenocytes (CASCM), mast cell colonies were observed. These colonies could be easily identified in situ under an inverted microscope because of their unique morphological characteristics, that is, they were burst colonies consisting of homogenous, round and refractile cells. Most of these colonies were confirmed by histochemical and ultrastructural analysis and by demonstration of presence of membrane receptors for IgE to consist entirely of mast cells. The mast cell colonies did not grown when CASCM and 2-mercaptoethanol (2-ME) were not present. It was also found that these colonies could be observed by the addition of 12-0-tetradecanoly phorbol-13-acetate (TPA) at high concentrations when CASCM but not 2-ME was present. These results show that the formation of mast cell colonies is absolutely dependent on some factor(s) present in CASCM and requires also the addition of 2-ME or TPA.

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Hypersensitivity pneumonitis was produced experimentally in guinea pig, and studied immunohistologically. Using bacterial α amylase (BαA) as the antigen, intramuscular immunization was performed every day for 5 days before final exposure through respiratory tract was carried out every day for two weeks. The pathological findings can be separated into four stages: 1) First stage (acute stage, bronchopneumonia like stage): There was acute inflammation surrounding respiratory bronchioles. 2) Second stage (evolution of alveolitis): There was alveolitis showing infiltration of lymphocytes and plasma cells in alveolar walls. 3) Third stage (granuloma formation): There were granulomatous lesions consisting of lymphocytes, histiocytes and plasma cells. 4) Fourth stage (stage of resolution): Resolution of granulomatous lesions had occurred. Localization of immunoglobulin deposits in the lung tissue, which was revealed by peroxidase-antiperoxidase method, correlated with the pathological findings. Deposits of IgG were detected along the alveolar walls in the first and the second stages, and these amounts increased as the stage advanced. In the granuloma stage, however, no deposits of immunoglobulin were discernible. Thus the formation of alveolitis was thought to have resulted from the deposition of immunoglobulin. However, the development of granuloma is difficult to explain by humoral immunity alone; it seems likely that some other mechanism, such as cellular immunity, is also be involved.

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