Elicitation of delayed-type hypersensitivity responses to poly(L-Tyr,LGlu)-poly(DLAla)--poly(LLys) by anti-idiotypic antibodies.

Strassmann, Gideon; Lifshitz, Ruth; Mozes, Edna

doi:10.1084/jem.152.5.1448

Cited by 12 publications

(2 citation statements)

References 10 publications

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“…Anti-idiotypic antibodies can be used to elicit DTH responses induced by the respective antigen. This was already shown with a conventional anti-idiotype serum against anti-poly-(LTyr,Glu)-poly-D,L-Ala--poly-L-Lys (T,G)--A-L) antibodies (11). We have used monoclonal antibodies against the PC-binding myeloma protein HOPC-8 to elicit DTH to PC.…”

Section: Discussionmentioning

confidence: 79%

Elicitation of delayed-type hypersensitivity to phosphorylcholine by monoclonal anti-idiotypic antibodies in an allogeneic environment.

Arnold¹,

Wallich²,

Hämmerling

1982

The Journal of Experimental Medicine

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Delayed-type hypersensitivity (DTH) to phosphorylcholine (PC) could be elicited by mixtures of monoclonal anti-idiotypic antibodies. Using this system in DTH transfers, the question was asked of whether anti-idiotypic antibodies could elicit antigen induced DTH in H-2-incompatible mice. Transfer of PC-activated BALB/c lymph node cells into BALB.K mice and subsequent elicitation with anti-idiotypic antibodies resulted in a positive DTH response. In contrast, elicitation with the antigen PC showed the expected H-2 restriction.

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Section: Discussionmentioning

confidence: 79%

Elicitation of delayed-type hypersensitivity to phosphorylcholine by monoclonal anti-idiotypic antibodies in an allogeneic environment.

Arnold¹,

Wallich²,

Hämmerling

1982

The Journal of Experimental Medicine

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“…To rule out the possibility that the anti-Id-induced blocking of DTH was not caused by the activation of suppressor cells, the mice were treated with doses of CY known to deplete suppressor T cell precursors (19)(20)(21)(22)(23)(24). Irrespective of the treatment to mice with CY, DTH induced in normal as well as in tyr(TMA)-immune mice was effectively blocked with anti-Id (Table III), suggesting the presence of Id on TDTH as observed in other systems (25,26). Direct evidence for the function of the idiotypic component of TDTH in tyr(TMA)-immune mice comes from experiments involving treatment of TDTH with anti-Id + C before adopti.ve transfer into naive recipients.…”

Section: Discussionmentioning

confidence: 81%

Hapten-specific responses to the phenyltrimethylamino hapten. III. Mice whose delayed-type hypersensitivity responses cannot be abrogated by the presence of anti-idiotypic suppressor T cells lack a critical modulatory T cell function.

Jayaraman¹,

Bellone²

1982

The Journal of Experimental Medicine

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The immune system normally appears to exist in a stable, steady state. As proposed by Jerne (1), the stability of the immune system is in part the result of a network of interactions involving idiotypes (Id) 1 and anti-idiotypes (anti-Id). Several systems have described a critical requirement of Id recognition in the induction of antibody synthesis (2-6). Evidence has also accumulated in recent years (7,8) indicating that Id-related mechanisms play a role in pathways among interacting T cells that eventually suppress hapten-specific delayed-type hypersensitivity (DTH). The downregulation of the immune response by suppressor T cells (Ts) is complex and not fully understood. Recent reports describing the heretofore unrecognized immunoregulatory functions of T cells such as "contrasuppressors" (9) and "abrosuppressors" (10) add still more to the complexity involved in the biological function, immunoregulation.In an effort to understand the role of the idiotypic network in the regulation of the immune response to a small synthetic antigen r-tyrosine-p-azophenyltrimethylammonium [tyr(TMA)], we have been studying the regulation of antibody and DTH responses directed to the TMA hapten. In the course of the study, we found that a single injection of tyr(TMA) in Freund's complete adjuvant (FCA) induced Ts that shut down only the cross-reactive Id + component of the anti-TMA antibody response (11). Recently (12), we have characterized the tyr(TMA)-induced T, and directly demonstrated the idiotype specificity of these cells by absorption procedures. Further, we demonstrated that these anti-idiotypic second-order Ts (T,2) cells (8) can also shut down DTH reactions (12) in addition to Id + antibody formation (11). The regulatory function of these cells on TMA-specific DTH responses was shown by adoptive transfer into naive recipients. However, when the anti-idiotypic T~-bearing mice were themselves immunized and tested for TMA specific DTH, they unexpectedly exhibited normal responses. Thus, although the anti-idiotypic T, could readily suppress DTH upon transfer to normal recipients, these same cells could not function intrinsically.

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The T‐cell receptor as analyzed by functional T‐cell lines specific to a synthetic polypeptide antigen

Mozes

1983

Biopolymers

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For a better understanding of the molecular nature of the antigen‐specific T‐cell recognition system, continuous T‐cell lines specific to the synthetic polypeptide antigen poly(Tyr,Glu)‐poly(DLAla)‐‐poly(Lys) [(T,G)–A‐‐L] were established from C3H.SW (high‐responder) activated T‐cells, cloned, and characterized. These lines and their derived clones are also constitutive secretors of antigen‐specific T‐cell replacing helper factors. The secreted T‐cell helper factor was shown to possess MHC determinants as well as V‐region determinants, or more specifically, idiotypic determinants that are cross‐reactive with those expressed on (T,G)–A‐‐L‐specific antibodies of the same mouse strain. Using the fluorescence‐activated cell sorter (FACS II) and individual C57BL/6 anti‐idiotypic sera produced against (T,G)–A‐‐L‐specific antibodies of C3H.SW origin, we have demonstrated the expression of the cross‐reactive idiotypic markers on the monoclonal helper T‐cells. Attempts were made to purify the active fraction of the T‐cell factors secreted by the (T,G)–A‐‐L continuous helper lines. Gel analysis of the twice affinity‐purified eluate of a (T,G)–A‐‐L column revealed the existence of iodinated bands with molecular weight of 17,000 and 15,000, in addition to a diffuse band of high molecular weight. The specific helper activity of the factors was associated with a 65–75% ammonium sulfate precipitate. Gel electrophoresis of the latter fraction, as well as of an eluate of a (T,G)–A‐‐L–Sepharose column indicated that a high‐molecular‐weight (< 67,000) and a low‐molecular‐weight (15,000–17,000) fraction contained the biological activity of the factor. Similar results were obtained following chromatography of the factor on Sephadex G‐100 columns. The two fractions were shown to be synthesized by the T‐cell lines, as indicated by internal labeling experiments using 35S‐methionine. Thus, it is suggested that a fraction of an apparent molecular weight of 15,000–17,000 preserves both the antigen specificity and the helper activity of the factor produced by the (T,G)–A‐‐L‐specific T‐cell lines.

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Elicitation of delayed-type hypersensitivity responses to poly(L-Tyr,LGlu)-poly(DLAla)--poly(LLys) by anti-idiotypic antibodies.

Cited by 12 publications

References 10 publications

Elicitation of delayed-type hypersensitivity to phosphorylcholine by monoclonal anti-idiotypic antibodies in an allogeneic environment.

Elicitation of delayed-type hypersensitivity to phosphorylcholine by monoclonal anti-idiotypic antibodies in an allogeneic environment.

Hapten-specific responses to the phenyltrimethylamino hapten. III. Mice whose delayed-type hypersensitivity responses cannot be abrogated by the presence of anti-idiotypic suppressor T cells lack a critical modulatory T cell function.

The T‐cell receptor as analyzed by functional T‐cell lines specific to a synthetic polypeptide antigen

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