Administration of nonimmunogenic 2,4-dinitrophenyl (DNP) conjugates of copolymers of D or L-glutamic acid and lysine (GL) induces hapten-specific tolerance in nonimmune and DNP-ovalbumin-primed strain 13 guinea pigs. This tolerant state is evidenced by depressed anti-DNP antibody synthesis in response to challenge with DNP-ovalbumin and by a diminished frequency of DNP-specific antigen-binding cells and of anti-DNP antibody-secreting cells. Such a nonimmunogenic compound (DNP-D-GL) will nevertheless elicit a DNP-specific anamnestic antibody response when administered at an appropriate time to DNP-ovalbumin-primed guinea pigs undergoing a graft-versus-host reaction. These experiments are discussed in terms of a two-cell theory of stimulation of antibody responses.

https://rupress.org/jem/article-pdf/134/1/201/1084279/201.pdf

Carrier function in anti-hapten antibody responses. IV. Experimental conditions for the induction of hapten-specific tolerance or for the stimulation of anti-hapten anamnestic responses by "nonimmunogenic" hapten-polypeptide conjugates.

Acquired tolerance to BSA in rabbits was terminated following the injection of certain preparations of altered BSA. Injections of Freund's adjuvant containing BSA complexed to anti-BSA, heat-denatured BSA, acetyl-BSA, picryl-BSA, or arsanil-BSA failed to terminate the tolerant state. Except in an occasional tolerant rabbit, injections of these preparations failed to cause the production of precipitating antibody to the altered preparation. Similar results were obtained following injections of alum-precipitated preparations of pepsin-degraded BSA, acetyl-BSA, and picryl-BSA. Injections of Freund's adjuvant containing sulfanil-BSA terminated the tolerant state, but only small amounts of non-precipitating anti-BSA were produced. Injections of Freund's adjuvant containing picryl-acetyl-BSA terminated the tolerant state in two of six rabbits, but again, only small amounts of non-precipitating anti-BSA were produced. Injections of an alum-precipitated preparation of picryl-acetyl-BSA failed to terminate the tolerant state. On the other hand, injections of Freund's adjuvant containing arsanil-sulfanil-BSA terminated the tolerant state in eleven of eleven rabbits and caused the production of precipitating anti-BSA in all nine of the rabbits tested. The tolerant state was terminated also in six of six rabbits injected with an alum-precipitated preparation of arsanil-sulfanil-BSA. Only one of these rabbits produced precipitating anti-BSA. In addition, the injection of BGG-tolerant rabbits with arsanil-BGG, sulfanil-BGG, or arsanil-sulfanil-BGG terminated the tolerant state. These results were discussed in relation to both the clonal selection theory of antibody production and autoimmunity.

https://rupress.org/jem/article-pdf/116/6/913/1080886/913.pdf

Termination of acquired immunological tolerance to protein antigens following immunization with altered protein antigens

Experiments and Results 117 A. Failure of Recovery of Ami-BSA Response in CBA Mice Thymectomised in Adult Life and Then Irradiated (Thymectomized-irradiated Mice) B. Restoration of Immune Response to Thymectomized-irradiated Mice with Thymus or Lymph-node Cells C. Depression of the Anti-BSA Response in Recipients of Transferred Cells Induced by Treatment of the Cell Donors with BSA; Effects of Duration of Treatment and Antigen Dosage on Lymph-node Cells or Thymus Cells D. Cooperation between Thymus and Marrow Cells in the Antibody Response to BSA E. Cooperation of Thymus Cells with Spleen Cells from Thymectomized-irradiated Mice F. Effect of BSA Treatment on Bone Marrow and Thymus; Controls for Antigen Carried Over to Recipients G. Retention of Radioactivity in Various Tissues after Injection of \"\"I-BSA H. Specificity of Paralysis of Thymus CeUs I. Effects of Long-term Paralysis J. Discussion of Results: Evidence That Antigen Carried Over with Thymus Cells Could not Account for Paralysis

Cellular Cooperation in the Antibody Response of Mice to Two Serum Albumins: Specific Function of Thymus Cells

Experiments with transgenic mice illustrate clonal elimination of T cells specific for antigens expressed appropriately in the thymus, but presence of inducible T cells when the antigen presented on class I MHC antigens is expressed exclusively on non-lymphohemopoietic cells in the periphery (pancreatic beta islet cells). TCR-transgenic LCMV-carrier mice expressing LCMV in the thymus exhibit clonal elimination at the early CD4+8+ thymocyte stage, causing CTL unresponsiveness in these mice. In contrast, studies with RIP LCMV-GP-transgenic mice (expressing GP in pancreatic beta cells) and with TCR-RIP LCMV-GP double-transgenic mice show that CTL reactivity is normal. These experiments argue against so-called peripheral anergy of class I MHC antigen-restricted cytotoxic T cells as a general mechanism of peripheral immunological tolerance to self. They reveal that self epitopes that are genetically self and presented by class I antigens may not be considered immunologically self if expressed solely extrathymically, despite the fact that they are antigenic and can be recognized by induced effector T cells. Genetic self that is presented on cells which can induce neither tolerance nor an immune response is immunologically dealt with as foreign and therefore may be called nonimmunological self. Appropriate presentation of the same epitope on antigen-presenting cells promptly induces effector T cells and causes disease; such disease should not be called autoimmune because it is an immunopathological T-cell mediated disease, comparable to an unfavorably balanced immunopathological T-cell response to a virus. Mechanisms that control autoantibody responses were studied in mice expressing a viral transgene. Such mice generate neutralizing antiviral autoantibody responses only when the transgenic viral antigen is linked to a foreign T-helper determinant. These findings, therefore, document differences in levels of T- vs B-cell tolerance (so-called split tolerance) under a given expression level of a "self" antigen. They illustrate how unresponsiveness of B cells to produce T-independent IgM is dose-dependent and that IgG autoantibodies are triggered by introducing foreign T-helper determinants that can be recognised in a linked fashion. This model suggests that, while T-cell tolerance to tolerogenic self in the thymus is solid, B-cell tolerance in general is not. From the point of view of autoantibody responses these T-helper cells may also be called immunopathological; i.e., these T-helper cells are specific for foreign epitopes that, via linked recognition, trigger truly autoimmune B cells.(ABSTRACT TRUNCATED AT 400 WORDS)

T and B cell tolerance and responses to viral antigens in transgenic mice: implications for the pathogenesis of autoimmune versus immunopathological disease.

Adult guinea pigs were made unresponsive to a heterologous protein (e.g. bovine gamma globulin, or BGG) or a hapten-protein conjugate (e.g. p-aminobenzoic acid-bovine gamma globulin, or PABAγmiddot;BGG) by intraperitoneal injection of 80 mg cyclophosphamide and the specific antigen. This immunologic unresponsiveness developed to the specific antigen administered simultaneously with the cyclophosphamide, and not to any variants. Thus, animals unresponsive to PABAγmiddot;BGG remained unresponsive to the original antigen on challenge with a variant, but formed delayed hypersensitivity and circulating antibody to the variant. The specificity of immunologic unresponsiveness, therefore, seems more closely related to the whole antigen molecule than does delayed hypersensitivity.

/pdf/the-specificity-of-allergic-reactions-vii-immunologic-3p48htwm6e.pdf

The specificity of allergic reactions vii. immunologic unresponsiveness, delayed hypersensitivity, and circulating antibody to proteins and hapten-protein conjugates in adult guinea pigs

The specificity of acquired immunological tolerance to azo proteins.

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The specificity of acquired immunological tolerance to azo proteins.