Rats immunized with a purified Ascaris suum allergen (Asc-1) or with its dinitrophenylated derivate (DNP-Asc-1) produced high levels of reaginic (IgE) antibodies. A second injection of antigen given 30 days later did not result in an anamnestic IgE antibody response. Immunization of adult-thymectomized, lethally-irradiated and bone-marrow reconstituted (ATxB) rats with soluble Asc-1 or DNP-Asc-1 failed to stimulate reaginic antibody production. The administration of glutaraldehyde-polymerized antigen induced in some but not all ATxB rats, low but detectable levels of IgE antibodies. These levels increased following a second injection of nonpolymerized antigen in Al(OH)3 gels. Priming of animals with poylmerized carrier and Bordetella pertussis did not stimulate a primary anticarrier IgE response but led to an enhanced antihapten IgE response following the administration of soluble DNP-Asc-1 in Al(OH)3. The results are consistent with the notion that a sharply reduced but clearly functional T-derived helper cell population could be triggered by the polymerized but not by the soluble form of the immunogen.
Sera obtained from rabbits after immunization with a variety of unrelated antigens contain antibodies that induce complement- (C) mediated lysis of sphingomyelin-containing liposomes in the absence of the relevant antigen from the membrane. Absorption or inhibition with dimyristoyl-phosphatidyl choline-containing liposomes were less effective than with sphingomyelin-containing liposomes in decreasing or abolishing C-dependent lysis of target-liposomes. Phosphoryl choline chloride inhibited the C-dependent lysis mediated by these antibodies, but only when used in high molar excess and in the presence of low antibody concentrations. Purified anti-liposome antibodies displayed an isoelectric focusing pattern consistent with a polyclonal response. The findings confirm the antibody nature of the anti-liposome activity of rabbit sera and indicate that their predominant specificity is directed against conformations of the phospholipid molecule in which the polar (phosphoryl choline) group does not have a major contribution.
Wistar/Furth rats were immunized with DNP-Asc-1 in various hapten-to-carrier ratios. The kinetics and intensity of the anti-DNP and anti-carrier IgE responses were dependent on the extent of carrier substitution. Lightly substituted conjugates induced excellent primary antihapten and anticarrier IgE antibodies while heavily substituted conjugates induced an early, short-lived and low antihapten response, but not anticarrier antibodies. The pattern of IgG antibody production was not dependent on the degree of substitution in the ranges tested. A single injection of carrier in CFA induced suppression of IgE antibodies following an injection with hapten-carrier conjugate, but enhanced the IgG antibody response to the hapten. Preimmunization or supplemental immunization with carrier in Al(OH)3 suppressed the IgE anti-DNP response but did not prevent the appearance of anticarrier antibodies. The suppression of the antihapten IgE response was also demonstrated in an adoptive transfer system when donors of carrier-primed spleen cells were injected with carrier in CFA or with carrier in Al(OH)3. On the other hand, excellent collaboration between carrier-primed helper cells and hapten-primed antibody-forming cell precursors was demonstrated for both IgE and IgG antibody production when donors of either carrier-primed or of hapten-primed cells received Bordetella pertussis as adjuvant. The results are consistent with the concept that intrinsic differences between the induction patterns of the IgE and IgG antibodies exist and that various factors contribute each in a different fashion to the dissociation of these responses.
Human myelin basic protein (MBP) was inserted into phosphatidyl-serine liposomes and Hartley guinea pigs were treated with 1 or 2 injections of MBP-liposomes mixture by the intracardial route before an encephalitogenic challenge with MBP in CFA. Other groups of guinea pigs were pretreated with equivalent amounts of MBP in saline or of MBP in IFA. Of 24 untreated animals, 22 developed EAE and died or had to be sacrificed within 15 days after challenge. Only 4 of 29 guinea pigs treated with either 75 microgram or 112 microgram MBP-liposomes developed clinical signs of the disease. In the group pretreated with MBP in saline, 11 of 15 animals died, whereas in the MBP-IFA group, only 4 out of 10 died. Histologic modifications were also decreased in the MBP-liposomes and MBP-IFA groups, but in many instances, clinical normal guinea pigs showed disseminated perivascular infiltrates in the brain and spinal cord. Delayed hypersensitivity reactions to MBP were positive in all but 1 animal tested. Early T-rosette levels followed essentially the clinical course of the disease: they were drastically decreased 7 days after challenge in the untreated and MBP-saline-treated groups, but remained essentially normal in the MBP-liposomes group throughout the experiment. Lymphocyte transformation tests carried out in parallel with soluble MBP and with MBP-liposomes indicated that animals in certain groups responded preferentially to 1 form or the other of the antigen. Compared with prevailing procedures, the single i.v. injection of a relatively small amount of liposome-associated MBP appears to represent a promising approach for the antigen-specific suppression of EAE.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.