Essential requirement of an invariant V alpha 14 T cell antigen receptor expression in the development of natural killer T cells.

Taniguchi, Masaru; Koseki, Haruhiko; Tokuhisa, Takeshi; Masuda, Kimio; Satō, Hiroshi; Kondo, Eisuke; Kawano, Tetsu; Cui, Junqing; Perkes, Alysia; Koyasu, Shigeo; Makino, Yuko

doi:10.1073/pnas.93.20.11025

Cited by 94 publications

(62 citation statements)

References 38 publications

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“…In 24␣␤ mice, the size of the transgenic thymi was 5-10% of WT, and the DP population was severely reduced. In TCR Va14 -transgenic mice, a reduction in thymocyte numbers was also seen (36,46). The number of thymocytes was reconstituted in the absence of the ligand CD1d, compatible with a deletion of cells during thymic selection due to CD1d autoreactivity of the transgenic TCR (47).…”

Section: Discussionmentioning

confidence: 76%

CD1d-Specific NK1.1+ T Cells with a Transgenic Variant TCR

Sköld

Faizunnessa

Wang

et al. 2000

The Journal of Immunology

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The majority of T lymphocytes carrying the NK cell marker NK1.1 (NKT cells) depend on the CD1d molecule for their development and are distinguished by their potent capacity to rapidly secrete cytokines upon activation. A substantial fraction of NKT cells express a restricted TCR repertiore using an invariant TCR Vα14-Jα281 rearrangement and a limited set of TCR Vβ segments, implying recognition of a limited set of CD1d-associated ligands. A second group of CD1d-reactive T cells use diverse TCR potentially recognizing a larger diversity of ligands presented on CD1d. In TCR-transgenic mice carrying rearranged TCR genes from a CD1d-reactive T cell with the diverse type receptor (using Vα3.2/Vβ9 rearrangements), the majority of T cells expressing the transgenic TCR had the typical phenotype of NKT cells. They expressed NK1.1, CD122, intermediate TCR levels, and markers indicating previous activation and were CD4/CD8 double negative or CD4+. Upon activation in vitro, the cells secreted large amounts of IL-4 and IFN-γ, a characteristic of NKT cells. In mice lacking CD1d, TCR-transgenic cells with the NKT phenotype were absent. This demonstrates that a CD1d-reactive TCR of the “non-Vα 14” diverse type can, in a ligand-dependent way, direct development of NK1.1+ T cells expressing expected functional and cell-surface phenotype characteristics.

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Section: Discussionmentioning

confidence: 76%

CD1d-Specific NK1.1+ T Cells with a Transgenic Variant TCR

Sköld

Faizunnessa

Wang

et al. 2000

The Journal of Immunology

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“…The following mAbs were used: anti-CD4, anti-CD44, anti-CD25, anti-CD69, anti-Fas, anti-FasL, anti-CTLA-4, anti-CD122, anti-V␤8.1, 8.2 (all from BD PharMingen, San Diego, CA), and anti-V␣14 (provided by Dr. M. Taniguchi, Department of Molecular Immunology, Graduate School of Medicine, Chiba University, Chiba, Japan) (26). KJ1-26 (provided by Dr. H. Ishikawa, Department of Microbiology, Keio University School of Medicine, Tokyo, Japan) recognizes Tg TCR specific to OVA.…”

Section: Mabs and Flow Cytometrymentioning

confidence: 99%

Administration of an Antigen at a High Dose Generates Regulatory CD4+ T Cells Expressing CD95 Ligand and Secreting IL-4 in the Liver

Watanabe

Yoshida

Shirai

et al. 2002

The Journal of Immunology

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Ags administered orally at a high dose are absorbed in immunogenic forms and perfuse the liver, which raises a question regarding the relevance of hepatic lymphocyte activation to the systemic hyporesponsiveness against the ingested Ag. Oral administration of 100 mg of OVA to the mice led to massive cell death of OVA-specific (KJ1-26+) CD4+ T cells by Fas-Fas ligand (FasL)-mediated apoptosis in the liver, which was associated with the emergence of hepatic KJ1-26+CD4+ T cells expressing FasL. Hepatic CD4+ T cells in OVA-fed mice secreted large amounts of IL-4, IL-10, and TGF-β1 upon restimulation in vitro and inhibited T cell proliferation. Adoptive transfer of these hepatic CD4+ T cells to naive mice and subsequent antigenic challenge led to suppression of T cell proliferation as well as IgG Ab responses to OVA; this effect was mostly abrogated by a blocking Ab to FasL. i.p. administration of an Ag at a high dose also generated hepatic CD4+FasL+ T cells with similar cytokine profile as T cells activated by oral administration of Ags at a high dose. Finally, we did not see an increase in FasL+ cells in the hepatic CD4+Vβ8+ T cell subset of MRL/lpr/lpr mice given staphylococcal enterotoxin B, indicating the requirement for Fas-mediated signals. These hepatic CD4+FasL+ regulatory cells may explain the tolerogenic property of the liver and play roles in systemic hyporesponsiveness induced by an Ag administered at a high dose.

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“…25 Based on our results and others, we speculate that ␣␤ T cells are indispensable, but that other cell types are also responsible for IL-12-mediated antitumor immunity. Because NK1 T cells cannot be generated in SCID mice 26 and NK cells are not deeply involved in the IL-12-mediated reaction, CD11b ϩ macrophages, for example, are one of the candidate cells that possibly contribute to the response.…”

Section: Antitumor Effect In Immunocompromised Hostsmentioning

confidence: 99%

Protective immunity is induced in murine colon carcinoma cells by the expression of interleukin-12 or interleukin-18, which activate type 1 helper T cells

et al. 2000

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We investigated the antitumor effects induced by the production of interleukin-12 (IL-12) or IL-18, which influence the function of T helper type 1 cells, in murine colon carcinoma cells (Colon 26). Retrovirally transduced cells with IL-12 genes that encoded both p35 and p40 (Colon 26/IL-12) lost their tumorigenicity when inoculated subcutaneously or intraperitoneally into syngeneic immunocompetent mice. Moreover, the mice that had rejected the Colon 26/IL-12 cells generated protective immunity to wild-type

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Essential requirement of an invariant V alpha 14 T cell antigen receptor expression in the development of natural killer T cells.

Abstract: NK1.1+ T [natural killer (NK) T] cells ex-press an invariant T cell antigen receptor a chain (TCRa) encoded by VCYl4 and Ja281 segments in association with a limited number of V,Bs, predominantly Vj88.

Cited by 94 publications

References 38 publications

CD1d-Specific NK1.1+ T Cells with a Transgenic Variant TCR

CD1d-Specific NK1.1+ T Cells with a Transgenic Variant TCR

Administration of an Antigen at a High Dose Generates Regulatory CD4+ T Cells Expressing CD95 Ligand and Secreting IL-4 in the Liver

Protective immunity is induced in murine colon carcinoma cells by the expression of interleukin-12 or interleukin-18, which activate type 1 helper T cells

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