Specific enrichment of the suppressor T cell bearing I-J determinants: parallel functional and serological characterizations.

Okumura, Katsuhiko; Takemori, Toshitada; Tokuhisa, Takeshi; Tada, Tomio

doi:10.1084/jem.146.5.1234

Cited by 101 publications

(45 citation statements)

References 20 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This finding favors the Ts of the KLH-specific Ts reported by Okumura et al (10). In addition, as reported by Tada et al (13) KLH-specific Ts are nylon-wool adherent.…”

Section: +supporting

confidence: 79%

“…The data in Table 2 show that the Ts of contact hypersensitivity are also nylon-wool adherent. From these results it seems likely that the nature of the syninduced Ts in DNFB-specific hypersensitivity is similar to that of the Ts of antibody production (10,14), except for the form of the antigen-binding receptors.…”

Section: +mentioning

confidence: 68%

“…Okumura et al (10) observed that KLH-specific Ts possess KLH-binding receptors. Miller (4) showed that the Ts induced by DNP-syngeneic LC could bind the membrane fraction of DNP-modified lymphoid cells, whereas his Ts did not bind with DNP-lysine or DNP-congeners columns.…”

Section: +mentioning

confidence: 99%

See 2 more Smart Citations

Genetic Control of Contact Hypersensitivity

Ishii

Ikezawa

Nagai

et al. 1981

Microbiology and Immunology

View full text Add to dashboard Cite

The characteristics of suppressor cells induced by 2,4-dinitrophenyl (DNP)-coupled syngeneic lymphocytes (syninduced suppressor cells) were studied. 2,4-dinitro-l-fluorobenzene (DNFB) contact hypersensitivity was completely suppressed when the syninduced suppressor cells were transferred intravenously. These syninduced suppressor cells had surface markers of Thy-l , FcR-and Lyt-Zf, 3+ antigens, as well as I-J gene products on their cell surfaces. The suppression of DNFB contact hypersensitivity was abrogated when these suppressor T cells were incubated in Petri dishes coated with the DNP-syngeneic lymphoid cell membrane, which suggests that these suppressor T cells had the specific antigen-binding receptors on their cell surfaces.Suppressor mechanisms in contact hypersensitivity to 2,4-dinitro-I-fluorobenzene (DNFB), 2,4, 6-trinitro-I-chlorobenzene (TNCB), oxazolone, and many other haptens have been widely studied. The surface marker of the 2, 4-dinitrophenyl (DNP)-specific syninduced suppressor cells has been reported to be Thy-I antigen-positive (6). The suppressor factors that suppress contact hypersensitivity to TNCB antigen have been shown to contain 1-J determinants (2). In addition, it has been determined that keyhole limpet hemocyanin (KLH)-specific suppressor T-cells (Ts) (10) and human gamma globulin (HGG)-specific Ts (14) belong to a population of 1-J+ and Lyt-Zt, 3+. Recently. Sy et al (12) reported that the suppressor T-cells that block the efferent route of contact hypersensitivity (Ts-eff') require the presence of another population of auxiliary sup-

show abstract

“…This finding favors the Ts of the KLH-specific Ts reported by Okumura et al (10). In addition, as reported by Tada et al (13) KLH-specific Ts are nylon-wool adherent.…”

Section: +supporting

confidence: 79%

Section: +mentioning

confidence: 68%

See 1 more Smart Citation

Genetic Control of Contact Hypersensitivity

Ishii

Ikezawa

Nagai

et al. 1981

Microbiology and Immunology

View full text Add to dashboard Cite

show abstract

“…variety of antigenic systems have been shown to involve T cells that bear determinants encoded by the I-J subregion of the H-2 gene complex (16,(23)(24)(25)(26). The I-J phenotype of pork insulin-specific suppressor cells was evaluated next.…”

Section: Requirement For I-j + Cells For Suppression Suppressor Pathmentioning

confidence: 99%

Regulatory mechanisms in immune responses to heterologous insulins. II. Suppressor T cell activation associated with nonresponsiveness in H-2b mice.

Jensen¹,

Pierce²,

Kapp³

1984

The Journal of Experimental Medicine

View full text Add to dashboard Cite

Murine antibody responses to insulins are controlled by MHC-linked Ir genes. Although mice of the H-2b haplotype do not make antibody in response to pork insulin, we demonstrate in this communication that immunization with pork insulin stimulates radioresistant, Lyt-1+2- helper T cells that are capable of stimulating secondary antibody responses to pork insulin in vitro, but that this activity is masked by radiosensitive, Lyt-1-2+, I-J+ suppressor T cells. The suppressor T cells, present after immunization with pork insulin but not beef insulin, suppress the secondary response to pork but not beef insulin. The amino acid sequences of pork and beef insulins differ only at the A-chain loop; thus, pork insulin-specific suppressor T cells appear to recognize the A-chain loop determinant of pork insulin. The amino acid sequences of mouse and pork insulin are identical in the A-chain loop, which suggests that these suppressor T cells may be self-reactive. If this interpretation is correct, these suppressor T cells could be involved in the maintenance of self-tolerance to insulin. Nevertheless, these data clearly demonstrate that genetically determined nonresponsiveness in H-2b mice is conferred by activation of dominant, insulin-specific suppressor T cells (Ts), rather than by a defect in the stimulation of insulin-specific helper T cells (Th).

show abstract

“…First, the antibody activity was tested on the suppressor T cells of various strains of mice by a cytotoxic assay. It has been demonstrated that antigen-specific suppressor T cells enriched by antigen-coated dishes or columns bear the I-J products (13,14). By using the enriched suppressor T cells, it is clearly demonstrated in Fig.…”

Section: Discussionmentioning

confidence: 88%

Monoclonal antibodies that recognize the product controlled by a gene in the I-J subregion of the mouse H-2 complex.

Kanno¹,

Kobayashi²,

Tokuhisa³

et al. 1981

The Journal of Experimental Medicine

Self Cite

View full text Add to dashboard Cite

The product of gene(s) in the I-J subregion of the mouse H-2 complex that are expressed on allotype-specific and antigen-specific suppressor T cells has been defined (1; reviewed in 2). The soluble factors derived from antigen-specific suppressor T cells have also been found to bear the I-J subregion gene product (3-8). However, it has not been determined whether the I-J product on the antigen-specific suppressor T cells is the same as that on the antigen-specific suppressor T cell factor. Moreover, recent studies have shown that conventional anti-I-J alloantisera detect the cell surface markers on some helper T cells (9), concanavalin A (Con A)X-induced T cells (10) and some antigen-presenting cells (11). Tada et al. (9), especially, have demonstrated that the absorption of anti-I-J antisera with Lyt-l-positive splenic T cells resulted in the loss of ability to remove the helper (Th2) T cell function, whereas the absorbed anti-I-J still preserved the capacity to eliminate the suppressor activity. Thus, they proposed that the I-J product expressed on the antigen-specific suppressor T cells is distinct from that on the helper T cells. Therefore, it seems most likely that two or more genes rather than a single gene are accommodated in the l-J subregion.

show abstract

Specific enrichment of the suppressor T cell bearing I-J determinants: parallel functional and serological characterizations.

Cited by 101 publications

References 20 publications

Genetic Control of Contact Hypersensitivity

Genetic Control of Contact Hypersensitivity

Regulatory mechanisms in immune responses to heterologous insulins. II. Suppressor T cell activation associated with nonresponsiveness in H-2b mice.

Monoclonal antibodies that recognize the product controlled by a gene in the I-J subregion of the mouse H-2 complex.

Contact Info

Product

Resources

About