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Requirements for CD1d recognition by human invariant Valpha24+ CD4-CD8- T cells.

Exley M, Garcia J, Balk SP, Porcelli S - J. Exp. Med. (1997)

Bottom Line: Upon activation by anti-CD3 or CD1d, the clones produced both Th1 and Th2 cytokines.These results demonstrate that human invariant Valpha24+ CD4-CD8- T cells, and presumably the homologous murine NK1+ T cell population, are CD1d reactive and functionally distinct from NK cells.The conservation of this cell population and of the CD1d ligand across species indicates an important immunological function.

View Article: PubMed Central - PubMed

Affiliation: Cancer Biology Program, Hematology/Oncology Division, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA.

ABSTRACT
A subset of human CD4-CD8- T cells that expresses an invariant Valpha24-JalphaQ T cell receptor (TCR)-alpha chain, paired predominantly with Vbeta11, has been identified. A series of these Valpha24 Vbeta11 clones were shown to have TCR-beta CDR3 diversity and express the natural killer (NK) locus-encoded C-type lectins NKR-P1A, CD94, and CD69. However, in contrast to NK cells, they did not express killer inhibitory receptors, CD16, CD56, or CD57. All invariant Valpha24(+) clones recognized the MHC class I-like CD16 molecule and discriminated between CD1d and other closely related human CD1 proteins, indicating that recognition was TCR-mediated. Recognition was not dependent upon an endosomal targeting motif in the cytoplasmic tail of CD1d. Upon activation by anti-CD3 or CD1d, the clones produced both Th1 and Th2 cytokines. These results demonstrate that human invariant Valpha24+ CD4-CD8- T cells, and presumably the homologous murine NK1+ T cell population, are CD1d reactive and functionally distinct from NK cells. The conservation of this cell population and of the CD1d ligand across species indicates an important immunological function.

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Expression of NK-associated proteins by invariant Vα24+ T  cells. FACS® profiles of a representative DN invariant Vα24+ T cell clone  (DN2.C9) 4 wk after PHA stimulation. T cells were stained with mAbs  against the antigens shown or isotype-matched control mAb at 10 μg/ml  and with anti-IgG FITC conjugate for 30 min each before FACS® analysis with propidium iodide gating on viable cells. (Top, left to right) P3 isotype control (open histogram) and Vα24 (solid histogram), NKR-P1A,  CD69, CD94. (Bottom, left to right) p58 KIR (GL183 shown), CD16,  CD56, CD57.
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Figure 2: Expression of NK-associated proteins by invariant Vα24+ T cells. FACS® profiles of a representative DN invariant Vα24+ T cell clone (DN2.C9) 4 wk after PHA stimulation. T cells were stained with mAbs against the antigens shown or isotype-matched control mAb at 10 μg/ml and with anti-IgG FITC conjugate for 30 min each before FACS® analysis with propidium iodide gating on viable cells. (Top, left to right) P3 isotype control (open histogram) and Vα24 (solid histogram), NKR-P1A, CD69, CD94. (Bottom, left to right) p58 KIR (GL183 shown), CD16, CD56, CD57.

Mentions: The relationship between invariant Vα24+ DN T cells and NK cells was explored using a panel of mAbs recognizing proteins expressed predominantly by NK cells. Humans appear to have only a single NK1-like gene, the homologue of murine NKR-P1A, that is expressed by NK cells and, at low levels, by a subpopulation of peripheral blood T cells (33). Nonetheless, NKR-P1A was expressed at high levels by each of the invariant Vα24+ clones (Table 2 and Fig. 2), but not by any of the CD4+ Vα24+Vβ11+ clones that did not express the invariant Vα24-JαQ rearrangement (data not shown).


Requirements for CD1d recognition by human invariant Valpha24+ CD4-CD8- T cells.

Exley M, Garcia J, Balk SP, Porcelli S - J. Exp. Med. (1997)

Expression of NK-associated proteins by invariant Vα24+ T  cells. FACS® profiles of a representative DN invariant Vα24+ T cell clone  (DN2.C9) 4 wk after PHA stimulation. T cells were stained with mAbs  against the antigens shown or isotype-matched control mAb at 10 μg/ml  and with anti-IgG FITC conjugate for 30 min each before FACS® analysis with propidium iodide gating on viable cells. (Top, left to right) P3 isotype control (open histogram) and Vα24 (solid histogram), NKR-P1A,  CD69, CD94. (Bottom, left to right) p58 KIR (GL183 shown), CD16,  CD56, CD57.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2198960&req=5

Figure 2: Expression of NK-associated proteins by invariant Vα24+ T cells. FACS® profiles of a representative DN invariant Vα24+ T cell clone (DN2.C9) 4 wk after PHA stimulation. T cells were stained with mAbs against the antigens shown or isotype-matched control mAb at 10 μg/ml and with anti-IgG FITC conjugate for 30 min each before FACS® analysis with propidium iodide gating on viable cells. (Top, left to right) P3 isotype control (open histogram) and Vα24 (solid histogram), NKR-P1A, CD69, CD94. (Bottom, left to right) p58 KIR (GL183 shown), CD16, CD56, CD57.
Mentions: The relationship between invariant Vα24+ DN T cells and NK cells was explored using a panel of mAbs recognizing proteins expressed predominantly by NK cells. Humans appear to have only a single NK1-like gene, the homologue of murine NKR-P1A, that is expressed by NK cells and, at low levels, by a subpopulation of peripheral blood T cells (33). Nonetheless, NKR-P1A was expressed at high levels by each of the invariant Vα24+ clones (Table 2 and Fig. 2), but not by any of the CD4+ Vα24+Vβ11+ clones that did not express the invariant Vα24-JαQ rearrangement (data not shown).

Bottom Line: Upon activation by anti-CD3 or CD1d, the clones produced both Th1 and Th2 cytokines.These results demonstrate that human invariant Valpha24+ CD4-CD8- T cells, and presumably the homologous murine NK1+ T cell population, are CD1d reactive and functionally distinct from NK cells.The conservation of this cell population and of the CD1d ligand across species indicates an important immunological function.

View Article: PubMed Central - PubMed

Affiliation: Cancer Biology Program, Hematology/Oncology Division, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA.

ABSTRACT
A subset of human CD4-CD8- T cells that expresses an invariant Valpha24-JalphaQ T cell receptor (TCR)-alpha chain, paired predominantly with Vbeta11, has been identified. A series of these Valpha24 Vbeta11 clones were shown to have TCR-beta CDR3 diversity and express the natural killer (NK) locus-encoded C-type lectins NKR-P1A, CD94, and CD69. However, in contrast to NK cells, they did not express killer inhibitory receptors, CD16, CD56, or CD57. All invariant Valpha24(+) clones recognized the MHC class I-like CD16 molecule and discriminated between CD1d and other closely related human CD1 proteins, indicating that recognition was TCR-mediated. Recognition was not dependent upon an endosomal targeting motif in the cytoplasmic tail of CD1d. Upon activation by anti-CD3 or CD1d, the clones produced both Th1 and Th2 cytokines. These results demonstrate that human invariant Valpha24+ CD4-CD8- T cells, and presumably the homologous murine NK1+ T cell population, are CD1d reactive and functionally distinct from NK cells. The conservation of this cell population and of the CD1d ligand across species indicates an important immunological function.

Show MeSH
Related in: MedlinePlus