Concanavalin A-induced suppressor cells.
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Biomedical subjects
Publications and source records attributed to J G Armitstead.
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The rise in plasma adenosine-3',5'-monophosphate occurring in response to insulin induced hypoglycaemia in normal human subjects, was abolished by non-selective beta-adrenoceptor blockade but unaffected by selective beta 1-adrenoceptor blockade. This implies that the rise is secondary to beta 2-adrenoceptor stimulation. The abolition of this rise by non-selective beta-adrenoceptor blockade had no pronounced effect on the recovery from hypoglycaemia. Endogenous opiate receptor blockade with naloxone had no significant effect on the recovery from insulin induced hypoglycaemia, or the hormonal mechanisms involved.
Suppressor T cell function and the sensitivity of lymphocyte transformation to histamine has been studied in 9 atopic patients with high serum IgE levels and in 14 controls. The effect of concanavalin A (Con A) induced suppressor T cells on the proliferative response of fresh lymphocytes to mitogens and antigens was measured; in atopic subjects the median suppression to 5.0 micrograms/ml Con A was 80% to 1.0 microgram/ml Phytohaemagglutinin (PHA) was 73%, to Dermatophagoides pteronyssinus extract was 45% and to streptokinase--streptodornase was 24%. Indomethacin increased lymphocyte proliferation to mitogens, but to a variable degree, in both groups. Histamine suppressed lymphocyte transformation to PHA and Con A (median suppression in normal subjects 38 and 46%, and in atopics 51 and 60%) and to D. Pteronyssinus extract. There was no significant difference between normal subjects and atopics in any of these functional assays. The relative and absolute numbers of total T cells, helper T cells and suppressor T cells measured by monoclonal antibodies and the helper to suppressor T cell ratio were normal in the atopic group. These results show that the activity of Con A induced suppressor T cells and the effect of histamine and indomethacin on lymphocyte proliferation is normal in highly atopic subjects. No suppressor T cell defect has been identified using these assays.