scholarly journals LYMPHOID CELLS IN DELAYED HYPERSENSITIVITY

1972 ◽  
Vol 135 (4) ◽  
pp. 985-996 ◽  
Author(s):  
S. B. Salvin ◽  
J. Nishio

X-irradiation up to 480 R does not inhibit either adoptive transfer of delayed hypersensitivity or production in vitro of soluble mediators, such as migration-inhibitory factor (MIF). Above that dosage and as high as 3000 R, adoptive transfer is inhibited, but production of MIF is not. An increase in skin response occurred when 24–48 hr were allowed to elapse after intravenous transfer and before skin testing. Treatment of recipients with colchicine at the time of adoptive transfer inhibited the development of a skin reaction to specific antigen.


1971 ◽  
Vol 133 (2) ◽  
pp. 187-201 ◽  
Author(s):  
Robert C. Bast ◽  
Eleanor J. Manseau ◽  
Harold F. Dvorak

Lymph node cells from guinea pigs immunized with HSA in complete Freund's adjuvant were grown in cultures containing different concentrations of specific antigen. Stimulation of thymidine incorporation was induced with progressively lower concentrations of HSA at successive intervals after sensitization. Moreover, the intensity of delayed skin reactions and the magnitude of stimulation in vitro increased over the same interval. These events are considered compatible with an evolution of the cellular immune response resulting from the selection of lymphoid cells by decreasing concentrations of antigen in vivo. Cells from animals rendered tolerant to HSA failed to respond to specific antigen in culture. As tolerance waned, stimulation was achieved at high but not low antigen concentrations. Tolerance, measured by cutaneous reactivity or by lymphocyte stimulation, was less readily induced in animals sensitized with adjuvant containing a reduced concentration of mycobacteria. Lymph nodes from these animals contained a large population of cells reactive at high antigen concentration, presumably less susceptible to the toleragenic effect of intravenous antigen. The dissociation of delayed hypersensitivity and antibody formation observed early in the immune response and upon recovery from tolerance has permitted correlation of lymphocyte stimulation with delayed hypersensitivity and cutaneous basophil hypersensitivity respectively.



1968 ◽  
Vol 128 (6) ◽  
pp. 1255-1265 ◽  
Author(s):  
Nancy H. Ruddle ◽  
Byron H. Waksman

Damage of rat embryo fibroblasts in the presence of sensitized lymph node cells reacting with specific antigen was shown to be closely correlated with delayed hypersensitivity in the animals from which the lymph node cells were taken. The phenomenon was not correlated with Arthus reactivity. In. animals sensitized with picryl conjugates of ovalbumin or human serum albumin, skin reactivity and the in vitro cytotoxic effect could be elicited only with the homologous conjugate or the protein carrier alone and not with picryl conjugates of heterologous proteins. Lewis rats developed more intense delayed sensitivity than BN rats, and Lewis lymph node cells were correspondingly more effective in producing specific damage of both syngeneic and allogeneic fibroblasts.





1973 ◽  
Vol 137 (6) ◽  
pp. 1494-1510 ◽  
Author(s):  
S. Michael Phillips ◽  
Burton Zweiman

The mechanism of suppression, of delayed hypersensitivity to tuberculoprotein by 6-mercaptopurine (6-MP) was studied in guinea pigs. Under the conditions of the protocol, suppression of tuberculin delayed skin test reactivity was not associated with a significantly altered end-organ response to mediators of permeability. No significant alteration of in vivo lymphoid activity, as measured by reconstitution studies, was found. In addition, lymphoid cells from 6-MP-treated animals reacted in a fashion similar to those of placebo-treated animals with respect to (a) antigen-induced lymphocyte proliferation, (b) antigen-induced liberation of macrophage inhibitory factor activity, (c) direct inhibition by antigen of peritoneal exudate cell migration. Conversely, suppression was seen in levels of blood monocytes and in vitro function of macrophages from 6-MP-treated animals in several respects: (a) adherence to glass, (b) migratory rate, (c) phagocytic capacity. Therefore, it would appear that a ma]or mechanism of 6-MP-induced suppression of delayed hypersensitivity is through its action on effector cells.



1964 ◽  
Vol 120 (6) ◽  
pp. 1189-1200 ◽  
Author(s):  
John R. David ◽  
H. S. Lawrence ◽  
L. Thomas

Peritoneal exudate cells from animals exhibiting delayed hypersensitivity are inhibited from migrating in vitro by specific antigen. This inhibition is completely abolished by pretreatment of the sensitive cells with trypsin. The action of trypsin is prevented by soybean trypsin inhibitor. The results of experiments with mixtures of normal and sensitive cells suggest that trypsin alters an immunologic capacity of the sensitive cells. Trypsinized sensitive cells are capable of passively transferring delayed hypersensitivity and peritoneal cells taken from recipient animals are inhibited from migrating in vitro by specific antigen. These results suggest that the cells rapidly resynthesize the material removed by trypsin. The possible nature of the material removed by trypsin is discussed.



1957 ◽  
Vol 106 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Lowell A. Glasgow ◽  
Herbert R. Morgan

Guinea pigs experimentally infected with mumps virus develop a delayed, hypersensitive skin reaction following the intradermal injection of heat-inactivated mumps virus. This in vivo hypersensitivity is accompanied by a state of cellular hypersensitivity which can be demonstrated in vitro by the addition of mumps viral antigen to cultures of splenic macrophages, following which they become less motile and undergo lysis. These observations support the hypothesis that the state of hypersensitivity which develops early in mumps virus infections may have a role in the pathogenesis of the disease.



1965 ◽  
Vol 122 (6) ◽  
pp. 1125-1134 ◽  
Author(s):  
John R. David

Peritoneal cells from guinea pigs exhibiting delayed hypersensitivity are inhibited from migrating in vitro by specific antigen. This inhibition is prevented by the addition of puromycin to the culture medium. The amount of puromycin necessary to prevent the inhibition by antigen also suppressed the incorporation of C14-leucine into peritoneal cell protein. Additional evidence that the action of puromycin is due to its inhibition of protein synthesis has been obtained with analogues of puromycin; those that inhibit protein synthesis also prevent the action of antigen on the cells, while those analogues that do not inhibit protein synthesis have no effect. Actinomycin also prevents the inhibition of sensitive cells by antigen while chloramphenicol has no effect. The data indicate that the inhibition of sensitive cell migration by antigen requires active protein synthesis. The possible mechanisms by which inhibition of protein synthesis may influence the in vitro reactions of delayed hypersensitivity are discussed.



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