The T cell receptor Vβ6 domain imparts reactivity to the Mls-1a antigen

Kanagawa, Osami; Palmer, Ed; Bill, Jerome

doi:10.1016/0008-8749(89)90255-4

Cited by 113 publications

(43 citation statements)

References 25 publications

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“…anti-I-Ed (14.4.4, mouse, [30]), anti-Thy-1 (Jlj, rat, [311), anti-CD8 (TIBlOS, rat, ATCC Rockville USA), antLCD4 (GK1.5, rat, [32]), anti-CD~E (145.2C11, hamster, [33]), anti-Va8 (KT.50-4.5, rat, [341) anti-VP2 (R20.6.5, rat. [35]), anti-VP3 (KJ25, hamster, [36]), antiVf34 (KT4-10, rat, 1371)-anti-VP5 (MR9-4, mouse, [38]), anti-Vf36 (RR4-7, rat, [39]), anti-VP7 (TR310, rat, [401), anti-VP8 (F23.1, mouse, [41]), anti-VP8.1/2 (KJ16-133, rat, [42]), anti-Vp9 (MR10-2, mouse, [43]), anti-VplO (B21.5, rat, [35]), anti-VPll (RK3-15, rat, 1441) and anti-VPl4 (14-2, rat, [45] …”

Section: Antibody Reagents 'mentioning

confidence: 99%

Cross‐reactive trinitrophenylated peptides as antigens for class II major histocompatibility complex‐restricted T cells and inducers of contact sensitivity in mice. Limited T cell receptor repertoire

et al. 1995

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The induction of contact sensitivity in mice by hapten reagents such as trinitrochlorobenzene (TNCB) involves the activation of class II major histocompatibility complex (MHC)-restricted, hapten-specific, CD4+ T cells. Reports from different laboratories have indicated that the relevant antigenic epitopes in such reactions might include hapten-conjugated, MHC class II-associated peptides. This study for the first time directly demonstrates that hapten-peptides account for the majority of determinants recognized by trinitrophenyl (TNP)-specific CD4+ T lymphocytes. The sequences of those TNP carrier peptides do not have to be related to mouse proteins. Thus, we show that TNP-modified peptides derived from mouse IgG, pigeon cytochrome c or staphylococcal nuclease known to bind to I-Ab or from lambda repressor with specificity to I-Ad as well as TNP-proteins such as bovine serum albumin, ovalbumin or keyhole limpet hemocyanin all create class II-restricted hapten determinants for a number of TNP-specific T cell clones and hybridomas. All of these cells were induced with cells modified by trinitrobenzene sulfonic acid (TNBS). In addition, we present arguments indicating that individual TNP-specific helper T cells may cross-react with different TNP-peptides bound to identical class II molecules. Chemical treatment of antigen-presenting cells with TNCB or TNBS may thus result in a limited number of particularly repetitive immunodominant hapten epitopes. Immunodominant epitopes were also indicated by an overrepresentation of the TCR elements V beta 2 and V alpha 10 in I-Ab/TNP-specific T cells. Most importantly, however, we demonstrate that TNP attached to lysine 97 in the staphylococcal nuclease peptide 93-105 (i.e. a clearly "non-self" sequence) is able to prime mice for subsequent elicitation of contact sensitivity by TNCB in the absence of foreign protein. We take this to indicate that those TNP-peptide determinants defined by us as immuno-dominant are responsible for the induction of contact sensitivity to haptens.

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Section: Antibody Reagents 'mentioning

confidence: 99%

Cross‐reactive trinitrophenylated peptides as antigens for class II major histocompatibility complex‐restricted T cells and inducers of contact sensitivity in mice. Limited T cell receptor repertoire

et al. 1995

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“…The T cells were analyzed for the percent CD4+ T cells and for percent Vp6 expressingT cells by double staining with anti-CD4-FITC (RM4-4) (Pharmingen) and anti-VP6-PE (RR4-7) [32] (Pharmingen) labeled antibodies.…”

Section: Facs Analysismentioning

confidence: 99%

Endogenous retroviral superantigen presentation by B cells induces the development of type 1 CD4⁺ T helper lymphocytes

1993

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The endogenous retroviral superantigen, minor lymphocyte stimulating antigen (Mls 1a, encoded by Mtv-7), when presented by highly purified B cells induced the development of a highly polarized population of T helper (Th)1 cells from naive peripheral CD4+ T cells in vitro. Immobilized anti-V beta 6 antibodies similarly generated highly polarized, largely V beta 6+, Th 1 populations in vitro. In the presence of exogenous interleukin-4, both stimuli were capable of generating Th 2, rather than Th 1 populations. Mls 1a presentation by B cells in vivo led to the development of an equally polarized Th 1 population. Using monoclonal antibodies against interferon-gamma and transforming growth factor-beta, it was demonstrated that maximal Th 1 development with either stimulus in vitro was dependent on the endogenous production of these two cytokines. Thus, our results demonstrate that the retroviral encoded superantigen, Mls 1a, drives the development of Th 1 cells both in vitro and in vivo, and they suggest that B cell presentation does not, in itself, lead to the generation of Th 2 cells.

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“…For the assessment of T cell function, flat-bottom microtiter wells were incubated for 3 h at 37 "C with 100 pl of PBS containing 20 pg/ml of anti-CD3, anti-Vp8, anti-Vp11, antiv33, or anti-Vp6 (RR4-7; [25]), and washed three times before use. Triplicates of lo5 spleen cells were incubated for 3 days in culture medium (RPMI 1640, 10 % FCS, 50 mM 2-ME, 1 mM Hepes; antibiotics) containing 10 U/ml of human rIL-2.…”

Section: Proliferation Assaysmentioning

confidence: 99%

In vivo administration of interleukin‐2 turns on anergic self‐reactive T cells and leads to autoimmune disease

1992

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One major mechanism of self tolerance involves the deletion of T cell clones in the thymus. In athymic mice, tolerance to self antigens must be generated extrathymically. T cells with self-reactive receptors undergo either peripheral clonal deletion or become unresponsive (i.e. anergic). The unresponsive state of human and mouse T cell clones in vitro can be reversed by the addition of exogenous interleukin (IL)-2, thus transforming anergic T cells to an activated state. Here it is shown that the in vivo delivery of IL-2 to athymic BALB/c nu/nu mice abrogates the anergic state of self-reactive V beta 3+ and V beta 11+ T cells [which are normally deleted in the minor lymphocyte stimulatory (Mls)-1b-, I-E(+)-expressing euthymic counterparts]. Thus, V beta 3+ and V beta 11+ T cells from IL-2-treated nude mice proliferate in response to T cell receptor cross-linking and acquire effector functions as measured by their ability to deliver aid to B cells upon specific stimulation. This activation correlates with the development of autoimmune manifestations (DNA autoantibodies, rheumatoid factors, erythroleukopenia and minimal change nephritis) in these IL-2-treated mice.

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The T cell receptor Vβ6 domain imparts reactivity to the Mls-1a antigen

Cited by 113 publications

References 25 publications

Cross‐reactive trinitrophenylated peptides as antigens for class II major histocompatibility complex‐restricted T cells and inducers of contact sensitivity in mice. Limited T cell receptor repertoire

Cross‐reactive trinitrophenylated peptides as antigens for class II major histocompatibility complex‐restricted T cells and inducers of contact sensitivity in mice. Limited T cell receptor repertoire

Endogenous retroviral superantigen presentation by B cells induces the development of type 1 CD4⁺ T helper lymphocytes

In vivo administration of interleukin‐2 turns on anergic self‐reactive T cells and leads to autoimmune disease

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The T cell receptor Vβ6 domain imparts reactivity to the Mls-1a antigen

Cited by 113 publications

References 25 publications

Cross‐reactive trinitrophenylated peptides as antigens for class II major histocompatibility complex‐restricted T cells and inducers of contact sensitivity in mice. Limited T cell receptor repertoire

Cross‐reactive trinitrophenylated peptides as antigens for class II major histocompatibility complex‐restricted T cells and inducers of contact sensitivity in mice. Limited T cell receptor repertoire

Endogenous retroviral superantigen presentation by B cells induces the development of type 1 CD4+ T helper lymphocytes

In vivo administration of interleukin‐2 turns on anergic self‐reactive T cells and leads to autoimmune disease

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Endogenous retroviral superantigen presentation by B cells induces the development of type 1 CD4⁺ T helper lymphocytes