All of the 8 strains that were previously assumed to be nontoxigenic Clostridium botulinum type C were re-examined for their toxigenicity and were demonstrated by trypsinization of the culture filtrates to produce C₂ toxin under improved cultural conditions. One per cent glucose added to trypticase peptone medium enhanced C₂ toxin production. The larger the spore population, the higher the C₂ toxicity and when spore population was smaller than a level of 10⁴/ml, no C₂ toxicity was demonstrated. The C₂ toxin was produced only during sporulation and not during vegetative growth.

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Studies were made to determine the effect of UV-irradiation of herpes simplex virus (HSV) on Concanavalin A (Con-A) -mediated agglutination of 3T3 cells. There were three different phases of agglutination by Con-A of cells infected with HSV. The agglutinability began to increase from 3 or 4 hr, or 72 hr after exposure of cells to HSV. The early-appearing agglutinability was further divided into two phases, based on its sensitivity to metabolic inhibitors. These were tentatively called “Early 1 or inhibitor sensitive”, “Early 2 or inhibitor insensitive” and “Late” agglutinability.
“Early 1” agglutination, detected from 3 hr post infection (pi), was induced by treating cells with HSV, either active or UV-irradiated for less than 5 min and was inhibited when actinomycin D (1 μg/ml) or cycloheximide (50 μg/ml) was added to the cultures. “Early 2” agglutination began to increase from 4 hr pi when cells were inoculated with HSV irradiated for 7 to 20 min and was not affected by either inhibitor. HSV irradiated for 6 min failed to induce either agglutinability. “Late” agglutination, observed 72 hr pi, was detected in cultures which had been treated with HSV irradiated for 4 to 15 min. Among those, virus irradiated for 6 to 8 min was most efficient. HSV-transformed cells were also agglutinated without exception by low concentrations of Con-A.

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Guinea pig lymph node cells suspension (LNC-O) was filtered through a glass wool column and the effluent (LNC-G) was further filtered through a nylon column. In this effluent (LNC-NE) about 30 per cent of the lymphocytes was identified as non-rosette forming cells (non-RFC). The non-RFC fraction was separated from LNC-NE fraction by Ficol-Conray specific gravity centrifugation of effluent cells reacted previously to rabbit red blood cells (RRBC). The upper layer after centrifugation, designated non-RFC fraction, was separated. In this fraction 96% of the cells were lymphocytes and about 95% of them were non-RFC, which lacked receptors for rabbit red blood cells (RRBC) or EAC and detectable surface immunoglobulin by conventional techniques.
Though the response of the lymphocytes in the non-RFC fraction to mitogenic (Con-A, LPS) or antigenic stimulation was lower in comparison with that in RFC-rich fraction, the response of non-RFC to ConA exceeded the response to LPS.
These facts suggest that at least a portion of the non-RFC may be cells from the T-cell line.

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Experimental autoimmune thyroiditis could be produced in SMA, C3H/He and C57BL mice by repeated injection at intervals of 30 days of syngeneic thyroid extract mixed with the capsular polysaccharide of Klebsiella pneumoniae (CPS-K) as a powerful adjuvant. The sequence of the development of autoimmune thyroiditis was histologically followed using SMA strain of mice, in which the thyroid lesions were most marked. A single injection of the thyroid extract mixed with CPS-K induced interstitial infiltration of small lymphocytes and other mononuclear cells, and follicular architecture was partially damaged. At early times (5 to 12 days) after the secondary injection of the material, there were aggregation of polymorphonuclear neutrophilic leukocytes with formation of microabscesses in the follicles and hyaline degeneration of small vessels in the thyroid glands, suggesting that this stage of the thyroid lesions was expression of an Arthus reaction. The maximal severity of the thyroid lesions was reached at 30 days after the secondary injection. At this time, the thyroid lesions consisted of extensive infiltration of small lymphocytes, plasma cells and other mononuclear cells with complete loss of follicular architecture and mild proliferation of fibrous connective tissues. Even at 200 days after the secondary injection, there was no evidence of spontaneous regression and resolution of the thyroid lesions. Based on the histological findings, it seems likely that in our system cell-mediated immunity plays a dominant role in initiation and maintenance of thyroiditis and humoral antibodies do so in its aggravation.

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Normal macrophages were activated to antibody-dependent cytotoxic effector cells by in vitro treatment with the local anesthetic lidocaine. Experiments on the dose-response and time course of the effect of lidocaine showed that incubation of normal macrophages with 10 mM lidocaine for 10 min at 28 C was enough for induction of antibody-dependent cellular cytotoxicity. The activation by lidocaine was accompanied by enhanced phagocytosis of sheep red blood cells (SRBC) sensitized with anti-SRBC antiserum, but not enhanced ingestion of polystyrene latex particles (PLP). These findings suggest that lidocaine, which has various effects on cell membranes, induces some perturbation of macrophage membranes, resulting in activation of Fc receptor functions in antibody-dependent cytotoxicity and phagocytosis.

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