Immunological and bacteriological basis for vaccination against dental caries in rhesus monkeys.
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Biomedical subjects
Publications and source records attributed to T Lehner.
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High titres of immunoconglutinin activity (antibody to bound complement components) have been found in the parotid, sublingual and submandibular saliva of most healthy subjects. The immunoconglutinin (IK) titre in mixed saliva was substantially lower than in the other samples of saliva. C3 was detectable in only three of 164 samples of parotid, submandibular and sublingual saliva but was present in forty-seven of 117 mixed saliva samples. It is suggested that crevicular fluid is the major source of C3 in mixed saliva. A negative correlation was found in mixed saliva between the C3 concentration and the IK titre, and this suggested that C3 was the inhibitor of IK in mixed saliva. Binding of C3 to IK has been demonstrated in mixed saliva by using highly purified salivary IK and C3. Purified C3, C3i, C3c and C3d inhibited the activity of purified IK. It is suggested that salivary IK represents the secretion of a B-lymphocyte population which has evaded the mechanism responsible for inducing B-cell tolerance to autologous serum proteins. The reason for its persistence in the salivary glands, however, is not known at present.
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Cell-mediated and humoral immune responses to Herpesvirus hominis type 1 (HVH1) and Candida albicans were studied in patients with leukoplakia, showing a histological spectrum of changes from epithelial keratosis to acanthosis and atypia, and in patients with carcinoma. The results were ranked according to increasing values of stimulation indices of lymphocyte transformation to HVH1, and the corresponding macrophage migration inhibition indices, and complement fixing antibody titres of each patient were correlated. This revealed that most patients with epithelial atypia were clustered to that end of the spectrum which had the highest stimulation and migration indices to HVH1; this relationship was not evident with C. albicans. In patients with keratosis and acanthosis there was a significant lack of correlation between lymphocyte transformation and migration inhibition to both HVH1 and C. albicans. In carcinoma the indices of lymphocyte transformation and migration inhibition to HVH1 and C. albicans were depressed. Furthermore, a significant negative correlation was found between lymphocyte transformation and migration inhibition to HVH1, unlike the positive correlation in control subjects. Complement fixing antibodies to HVH1, HVH2, cytomegalovirus and adenovirus, and fluorescent antibodies to C. albicans failed to show a significant change in titre in any one group of subjects tested. The results suggest a cell-mediated immune defect in leukoplakia, with a dissociation between lymphocyte transformation and macrophage migration inhibition to HVH1 and C. albicans in cases of keratosis or acanthosis. A specific increase in cell-mediated immunity to HVH1 in leukoplakia with epithelial atypia and the sequential changes argue in favour of a possible participation of HVH1 in carcinomatous transformation of some leukoplakias.
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The cell-mediated and antibody responses to Herpesvirus hominis type 1 were investigated in patients with primary and recurrent herpetic infections. Stimulation of lymphocyte transformation with the virus and the complement fixing antibody titre did not differ significantly between patients and controls. However, macrophage migration inhibition and lymphocyte cytotoxicity were impaired in patients. The defects were specific to H. hominis, as Candida oblicans, which was used as an unrelated antigen, failed to show a similar abnormality. These results and preliminary sequential studies suggest that the susceptibility to recurrent herpesvirus infection may be due to an impaired production of macrophage migration inhibition factor and lymphocyte cytotoxicity in the presence of intact lymphocyte sensitization and antibody formation.