Presence on idiotype-specific suppressor T cells of receptors that interact with molecules bearing the idiotype.

Owen, Frances L.; Ju, Shyr‐Te; Nisonoff, Alfred

doi:10.1084/jem.145.6.1559

Cited by 125 publications

(59 citation statements)

References 15 publications

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“…Studies from other laboratories have also demonstrated anti-idiotypic T cells involved in helper (21,22,(25)(26)(27) and suppressor (28)(29)(30)(31)(32)(33) cell activity. It might be envisioned that the anti-idiotypic T cell population could be divided into two distinct groups based on differences in the immunization procedures used to induce these cells and ultimately on differences in the specificity of the T ceils.…”

Section: Discussionmentioning

confidence: 99%

Antigen-specific helper T cells required for dominant production of an idiotype (THId) are not under immune response (Ir) gene control.

Bottomly¹,

Maurer²

1980

The Journal of Experimental Medicine

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Responder and nonresponder mice primed with poly-(L-glutamic acid,L-lysine,L-phenylalanine) (GLPhe), the response to which is under the control of immune response (Ir) genes, were used as a source of both types of helper T cells required for a T15 idiotype dominated T-dependent anti-phosphorylcholine (PC) response. It was found that the activity of one of the helper T cells needed for an anti-PC response was under major histocompatibility complex (MHC)-linked Ir gene control, and only GLPhe-primed responder mice could be used as a source of these cells. These T cells (ThMHC) whose presence is required for in vivo T-B collaboration are found in normal and anti-mu-treated mice, and their activity depends on the hapten being physically linked to the carrier molecule. By contrast, the activity of the second helper T cell (ThId) required for a T15-dominated anti-PC response was present in both GLPhe-primed responder and nonresponder mice. The ThId cell set that is missing or deficient in anti-mu treated mice can be restored by the addition of T cells from normal, carrier-primed donors and restimulating with the priming carrier. When T cells from GLPhe-primed donors are used as a source of ThId cells, both responder and nonresponder donors provide helper cells capable of inducing syngeneic B cells to produce a T15 dominated anti-Pc response. These results are interpreted to suggest that idiotype recognizing helper T cells (ThId) recognize antigen independent of known Ir gene products.

show abstract

Section: Discussionmentioning

confidence: 99%

Antigen-specific helper T cells required for dominant production of an idiotype (THId) are not under immune response (Ir) gene control.

Bottomly¹,

Maurer²

1980

The Journal of Experimental Medicine

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“…In most studies of idiotype-specific suppression of a B cell response, suppressor cells have been induced by administration of anti-idiotypic antiserum (7,10,19), idiotype alone (4,20), or idiotype conjugated to syngeneic cells (9). The operation of such an idiotypic suppressor mechanism during the normal course of a humoral immune response would be more directly demonstrated if antigen-induced suppressor cells, acting in an idiotype-specific manner, could be elicited by antigen.…”

mentioning

confidence: 99%

Hapten-specific T cell responses to 4-hydroxy-3-nitrophenyl acetyl. VII. Idiotype-specific suppression of plaque-forming cell responses.

Sherr¹,

Ju²,

Weinberger³

et al. 1981

The Journal of Experimental Medicine

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The ability of suppressor cells induced by the intravenous administration of 4-hydro-3-nitrophenyl acetyl (NP)-modified syngeneic cells to reduce an idiotypic B cell response was studied in both an in vivo and an in vitro system. Idiotype-positive B cells were assayed by the ability of guinea pig anti-idiotypic antiserum to specifically inhibit idiotype-positive plaque formation. It was found that up to 57% of the PFC response in vivo and 100% of the PFC response in vitro was inhibitable with antiidiotypic antiserum. The expression of these idiotype-positive B cells could be suppressed by the transfer of spleen cells form mice treated 7 d previously with NP coupled syngeneic cels. T cells are both required and sufficient for the transfer of idiotype specific suppression. The induction of these idiotype-specific T suppressor cells directly with antigen suggests that recognition of unique determinants on cell surfaces is important for regulation of lymphoid cell interactions. The role of idiotype-specific suppressor cells in the network of lymphoid interactions is discussed.

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“…In experiments in animals on the regulatory action of antiidiotypic antibodies, idiotypic suppression can result from direct interaction of the antiidiotypic antibodies with the receptor of the antibody-forming B cell, as well as from induction of idiotype-specific suppressor T cells (5,7,9,21). Idiotype-positive peripheral blood B cells may be precursors of the plasma cells that are localized in joint tissue and are producing RF (22,23).…”

Section: Discussionmentioning

confidence: 99%

Suppression of rheumatoid factor synthesis by antiidiotypic antibody in rheumatoid arthritis patients with cross‐reactive idiotypes

Takeuchi

Hosono

Koide

et al. 1985

Arthritis & Rheumatism

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The effect of antiidiotypic antibody on the in vitro production of rheumatoid factor was studied in rheumatoid arthritis patients with cross‐reactive idiotypic determinants. Antiidiotypic antibodies (ascites IgG) were developed against monoclonal rheumatoid factor (Ka m‐RF) by a cell fusion procedure. These antibodies were idiotype‐specific, since: 1) they reacted only with F(ab')2 fragment of Ka m‐RF; 2) they failed to react with normal IgM without rheumatoid factor activity; and 3) their F(ab')2 fragment inhibited the rheumatoid factor activity of Ka m‐RF. The antiidiotypic antibody strongly suppressed the in vitro production of rheumatoid factor by lymphocytes from unrelated rheumatoid arthritis patients with cross‐reactive idiotypes. The suppression was specific, since ascites IgG failed to suppress in vitro anti‐keyhole limpet hemocyanin antibody production by the lymphocytes. These results indicate that antiidiotypic antibody may influence the regulation of rheumatoid factor production in patients with rheumatoid arthritis.

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Presence on idiotype-specific suppressor T cells of receptors that interact with molecules bearing the idiotype.

Cited by 125 publications

References 15 publications

Antigen-specific helper T cells required for dominant production of an idiotype (THId) are not under immune response (Ir) gene control.

Antigen-specific helper T cells required for dominant production of an idiotype (THId) are not under immune response (Ir) gene control.

Hapten-specific T cell responses to 4-hydroxy-3-nitrophenyl acetyl. VII. Idiotype-specific suppression of plaque-forming cell responses.

Suppression of rheumatoid factor synthesis by antiidiotypic antibody in rheumatoid arthritis patients with cross‐reactive idiotypes

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