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Contact sensitization by epicutaneous application of picryl chloride causes in mice a significant reduction of the antibody responses to immunogenic TNP-conjugates. This split unresponsiveness is long-lasting. It was found that hapten applied on the skin became attached to the serum proteins and the transfer of such a serum into normal recipients, while not influencing the ability of these animals to become contact-sensitized to PC1, rendered them unable to mount the anti-TNP antibody response, Possible mechanisms of split unresponsiveness to the TNP determinant induced by PC1 treatment are suggested. [ABSTRACT FROM AUTHOR]

Alloxan diabetic BALB/c mice with high hyperglycaemia levels (⩾ 600 mg/100 ml) when immunized either with T-dependent (SRBC) or T-independent (TNP-LPS) antigens show a significant decrease in the number of specific PFC when compared with normo-glycaemic controls. Moderate diabetes (> 350 mg/100 ml) does not affect the immune response and in some experiments a slight increase of anti-SRBC plaques was seen. In transfer experiments primed spleen cells of either diabetic or normal donors gave much better responses when transferred to normal rather than diabetic X-irradiated recipients. In Mishell-Dutton (MD) cultures the anti-SRBC response of CBA spleen cells was moderately reduced only when the blood glucose level of cell donors exceeded 500 mg/100 ml. Glucose added to MD cultures of normal spleen cells diminished significantly the number of SFC when in concentrations exceeding 600 mg/100 ml. The data indicate that in diabetic animals B-lymphocyte function may be affected but give no clear-cut answer to whether this is also true for T-helper cells. Disabled lymphocytes, whatever population they represent, may partially recover when transferred into normo-insulinic milieu. It may be inferred that under conditions tested neither hyperglycaemia nor excess of corticosteroid accounted significantly for the impaired humoral responses in diabetic animals. These experiments imply, however, that in hypoinsulinaemia the lack of saturation of insulin receptors on the lymphocyte, and possibly also macrophage, membranes renders these cells functionally inactive presumably due to accumulation of cyclic AMP in the cell membrane. [ABSTRACT FROM AUTHOR]