scholarly journals Augmentation of delayed-type hypersensitivity by doses of cyclophosphamide which do not affect antibody responses.

1975 ◽  
Vol 141 (3) ◽  
pp. 697-702 ◽  
Author(s):  
P W Askenase ◽  
B J Hayden ◽  
R K Gershon
Keyword(s):  
T Cells ◽  
Antibody Responses ◽  
Delayed Type Hypersensitivity ◽  
Hypersensitivity Reactions ◽  
Low Doses ◽  
Hypersensitivity Response ◽  
Suppressor T Cells ◽  
Cyclophosphamide Treatment ◽  
Delayed Reactions ◽  
Foot Pad

Mice immunized with more SRBC than are required to produce optimal delayed-type hypersensitivity reactions, developed good antibody responses and poor delayed foot pad reactions. Cyclophosphamide treatment in low doses (20 mg/kg) before immunization, augmented the delayed-type hypersensitivity without affecting antibody responses. Cyclophosphamide did not augment delayed responses to optimal doses of SRBC (0.01%), but did augment the delayed hypersensitivity response of mice immunized with a suboptimal antigen dose (0.001%); which produced no detectable antibody response with or without cyclophosphamide pretreatment. These results suggest that antibody feedback is not the sole regulator of delayed reactions; the possibility that suppressor T cells may also be involved is discussed.

scholarly journals Antigen- and receptor-driven regulatory mechanisms. I. Induction of suppressor T cells with anti-idiotypic antibodies.

1979 ◽  
Vol 150 (5) ◽  
pp. 1216-1228 ◽  
Author(s):  
M S Sy ◽  
B A Bach ◽  
Y Dohi ◽  
A Nisonoff ◽  
B Benacerraf ◽  
...  
Keyword(s):  
T Cells ◽  
Suppressor Cells ◽  
Regulatory Mechanisms ◽  
Delayed Type Hypersensitivity ◽  
Low Doses ◽  
Spleen Cells ◽  
Suppressor T Cells ◽  
Humoral Antibodies ◽  
Coupled Cells ◽  
Immunoglobulin Molecule

Delayed-type hypersensitivity (DTH) to the azobenzenearsonate (ABA) hapten can be readily induced in A/J mice injecting ABA-coupled syngeneic spleen cells subcutaneously. To further characterize this T-cell-dependent immunological phenomenon, the effect of passively administered anti-cross-reactive idiotype common to anti-ABA antibodies of A/J mice (CRI) antibodies on the development of ABA-specific DTH was investigated. Animals given daily injections (of minute amounts) of anti-CRI antibodies subsequent to immunization with ABA-coupled cells show significant reduction of ABA specific responses. This inhibition is antigen specific and requires the intact immunoglobulin molecule, as F(ab')2 treatments were ineffective in suppressing the reaction. Investigations of the mechanism of the anti-CRI-induced suppression of ABA DTH revealed that the observed suppression is a result of the activation of suppressor cells. Spleen cells taken from animals which received anti-CRI antibodies were able to adoptively transfer suppression to naive recipients. This suppression was shown to be mediated by T cells, as anti-Thy1.2 plus complement completely abrogated the transfer of suppression. In addition, animals pretreated with low doses of cyclophosphamide were not suppressed by the administration of anti-CRI antibodies. The genetic restriction of anti-CRI-induced suppression was demonstrated. Antibodies to the major cross-reactive idiotype, (CRI) associated with anti-ABA antibodies in A/J mice were unable to suppress the development of DTH to ABA in BALB/c mice (H-2d, Igh-1a). Such antibodies were, however, fully active in suppressing ABA DTH in the allotype-congenic C.AL-20 strain which has an allotype (Igh-1d) similar to that of A/J (Igh-1e) on a BALB/c background, and which produces humoral antibodies with the CRI.

scholarly journals 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.

1982 ◽  
Vol 155 (6) ◽  
pp. 1810-1822 ◽  
Author(s):  
S Jayaraman ◽  
C J Bellone
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Population ◽  
Cell Function ◽  
Suppressor Cell ◽  
Delayed Type Hypersensitivity ◽  
Loss Of Function ◽  
Suppressor T Cells ◽  
T Cell Function ◽  
Cyclophosphamide Treatment

A single intraperitoneal injection of the monovalent synthetic antigen, tyrosinated trimethylaminoaniline [tyr(TMA)] in Freund's complete adjuvant induces an antiidiotypic second-order T suppressor (Ts2) cell population 6 wk later. This population was able to suppress TMA-specific delayed-type hypersensitivity (DTH) responses when adoptively transferred into normal syngeneic recipients. However, they failed to function intrinsically. The inability of the Ts2 to function intrinsically was not caused by compensating idiotype-negative T cells that mediate DTH. Rather, this paradoxical observation was found to be caused by the absence or loss of function of a critical modulatory T cell population in the suppressor cell-bearing mice. This cell is functionally active in normal mice immunized for DTH responses and is sensitive to cyclophosphamide treatment. In addition, this cell type bears idiotype on its surface and is Thy-1+ and Lyt-1-,2+. It was demonstrated that by adoptively transferring the activated modulatory T cells from normal mice into tyr(TMA)-immune recipients, it was possible to observe suppressor cell function intrinsically. The potential importance of modulatory T cell function in the regulation of antibody and DTH responses is discussed.

Naive T cells can mediate delayed-type hypersensitivity response in T cell receptor transgenic mice

1994 ◽  
Vol 24 (7) ◽  
pp. 1512-1516 ◽  
Author(s):  
Takehito Sato ◽  
Takeshi Sasahara ◽  
Yukitsugu Nakamura ◽  
Takako Osaki ◽  
Takanori Hasegawa ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Transgenic Mice ◽  
T Cell Receptor ◽  
Cell Receptor ◽  
Delayed Type Hypersensitivity ◽  
Hypersensitivity Response ◽  
Naive T Cells ◽  
Naïve T Cells ◽  
Delayed Type Hypersensitivity Response

scholarly journals Antigen- and receptor-driven regulatory mechanisms. II. Induction of suppressor T cells with idiotype-coupled syngeneic spleen cells.

1979 ◽  
Vol 150 (5) ◽  
pp. 1229-1240 ◽  
Author(s):  
M S Sy ◽  
B A Bach ◽  
A Brown ◽  
A Nisonoff ◽  
B Benacerraf ◽  
...  
Keyword(s):  
T Cells ◽  
Heavy Chain ◽  
Suppressor Cells ◽  
Significant Inhibition ◽  
Regulatory Mechanisms ◽  
Delayed Type Hypersensitivity ◽  
Spleen Cells ◽  
Suppressor T Cells ◽  
Specific Manner ◽  
Coupled Cells

Anti-p-azobenzenearsonate (ABA) antibodies, coupled covalently to normal syngeneic spleen cells and then given intravenously to normal animals, were found to be potent tolerogens for delayed-type hypersensitivity (DTH) to ABA. The ability of the antibody-coupled cells to induce tolerance was determined to be a result of the cross-reactive idiotype (CRI+) fraction of the antibodies, because anti-ABA antibodies lacking the CRI+ components when coupled to spleen cells were unable to cause any significant inhibition. Furthermore, genetic analysis revealed that the ability of CRI-coupled cells to inhibit ABA-specific DTH is linked to Igh-1 heavy chain allotype, in as much animals which possess heavy chain allotypes similar to that of A/J were sensitive to this inhibition. Adoptive transfer experiments provided evidence that CRI-coupled cells induce suppressor cells, and spleen cells or thymocytes from animals received CRI-coupled cells were able to transfer suppression to naive recipients. In addition, treatment with anti-Thy1.2 serum plus complement completely abrogated their ability to transfer suppression. Thus, this active suppression is a T-cell-dependent phenomenon. In investigating the specificity of these suppressor T cells, it was found that they functioned in an antigen-specific manner and were unable to suppress the development of DTH to an unrelated hapten 2,4-dinitro-1-fluorobenzene.

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