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Biomedical subjects

I Green

Publications and source records attributed to I Green.

223 records · Page 13Linked to original sources

The behavior of hapten-poly-L-lysine conjugates as complete antigens in genetic responder and as haptens in nonresponder guinea pigs.

30 to 40% of Hartley strain guinea pigs have previously been demonstrated to possess a dominant autosomal gene which enables them to recognize the antigenicity of hapten-poly-L-lysine conjugates as expressed by the development of both antihapten antibodies and delayed hypersensitivity to the immunizing antigen. In the present study, it was shown that PLL alone was weakly antigenic in such genetic responder animals. Immunization with DNP-PLL electrostatically combined with foreign albumins elicits the production of anti-DNP antibodies in all Hartley strain guinea pigs, although the percentage of animals demonstrating a delayed response to DNP-PLL and therefore considered genetic responders remains 30 to 40%. Immunization with nonantigenic polyanions combined with DNP-PLL does not produce such an effect. Some degree of PLL specificity of purified anti-DNP antibodies produced by genetic nonresponder animals by immunization with DNP-PLL combined with foreign albumins was demonstrated by means of fluorescence quenching.

Animals↗

Studies of immune functions of patients with systemic lupus erythematosus. I. Dysfunction of suppressor T-cell activity related to impaired generation of, rather than response to, suppressor cells.

T cell suppressor function in patients with systemic lupus erythematosus (SLE) was evaluated by studying the ability of concanavalin A- (Con A) activated T cells to suppress proliferative responses by responder cells autologous with the Con A-activated T cells. Impaired suppressor T-cell activity in patients with SLE was observed with regard to three effector functions: 1) the allogeneic response of T cells, 2) the Con A response of T cells, and 3) the B cell response to pokeweed mitogen (PWM). No defect was found with regard to suppression of the T-cell response to phytohemagglutinin (PHA). Mixing experiments between SLE and normal cells were carried out to further define the nature of the SLE suppressor defect. When responder cells from SLE patients were cultured with Con A-activated T cells from normal controls, the normal suppressor T cells caused suppression of SLE responder cells. In contrast, Con A-activated T cells from SLE patients were incapable of exerting suppressor effects on normal responder cells. These observations indicate that the impaired suppressor activity in SLE patients resides in the generation of suppressor T cells, rather than in the response to suppressor T cell signals.

B-Lymphocytes↗