The Contribution of NKT Cells, NK Cells, and Other γ-Chain-Dependent Non-T Non-B Cells to IL-12-Mediated Rejection of Tumors

Park, Seho; Kyin, Tim; Bendelac, Albert; Carnaud, Claude

doi:10.4049/jimmunol.170.3.1197

Cited by 49 publications

(30 citation statements)

References 25 publications

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“…They exerted their versatile roles in the defense of pathogens like murine cytomegalovirus (MCMV) [21,22] . Several studies also reported that hepatic NK and NKT cell took part in the antimetastasis of tumor [23][24][25] . NK1.1 + cells were reported to involve in the pathogenesis of many diseases, like human immunodeficiency virus (HIV) infection and liver disease [26,27] .…”

Section: Discussionmentioning

confidence: 99%

Isolation of murine hepatic lymphocytes using mechanical dissection for phenotypic and functional analysis of NK1.1⁺cells

Dong

Wei²,

Sun³

et al. 2004

WJG

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AIM:To choose an appropriate methods for the isolation of hepatic lymphocytes between the mechanical dissection and the enzymatic digestion and investigate the effects of two methods on phenotype and function of hepatic lymphocytes. METHODS:Hepatic lymphocytes were isolated from untreated, poly (I:C)-stimulated or ConA-stimulated mice using the two methods, respectively. The cell yield per liver was evaluated by direct counting under microscope. Effects of digestive enzymes on the surface markers involved in hepatic lymphocytes were represented by relative change rate [(percentage of post-digestionpercentage of pre-digestion)/percentage of pre-digestion]. Phenotypic analyses of the subpopulations of hepatic lymphocytes and intracellular cytokines were detected by flow cytometry. The cytotoxicity of NK cells from wild C57BL/6 or poly (I:C)-stimulated C57BL/6 mice was analyzed with a 4-h 51 Cr release assay. RESULTS:NK1.1 + cell markers, NK1.1 and DX5, were significantly down-expressed after enzymatic digestion and their relative change rates were about 28% and 32%, respectively. Compared with the enzymatic digestion, the cell yield isolated from unstimulated, poly (I:C)-treated or ConA-treated mice by mechanical dissection was not significantly decreased. Hepatic lymphocytes isolated by the mechanical dissection comprised more innate immune cells like NK, NKT and γδ cells in normal C57BL/6 mice.

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Section: Discussionmentioning

confidence: 99%

Isolation of murine hepatic lymphocytes using mechanical dissection for phenotypic and functional analysis of NK1.1⁺cells

Dong

Wei²,

Sun³

et al. 2004

WJG

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“…Generally, however, NKT cell-deficient mice are immune competent (24)(25)(26). There are also numerous reports suggesting activating or suppressing roles for NKT cells in many immune responses only on activation by specific ligands.…”

Section: Compared With Cd1dmentioning

confidence: 99%

Regulation of Secondary Antigen-Specific CD8+ T-Cell Responses by Natural Killer T Cells

et al. 2009

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The physiologic function of natural killer T (NKT) cells in adaptive immunity remains largely unknown because most studies have used NKT cell agonists. In the present study, the role of NKT cells during the secondary effector phase was investigated separately from the primary immunization phase via adoptive transfer of differentiated effector T cells into naive recipients. We found that secondary antitumor CD8 + T-cell responses were optimal when NKT cells were present. Tumor-specific CD8 + effector T cells responded less strongly to tumor cell challenge in NKT cell-deficient recipients than in recipients with intact NKT cells. NKT cell-mediated enhancement of the secondary antitumor CD8 + T-cell response was concurrent with increased number and activity of tumorspecific CD8 + T cells. These findings provide the first demonstration of a direct role for NKT cells in the regulation of antigen-specific secondary T-cell responses without the use of exogenous NKT cell agonists such as A-galactosylceramide (A-GalCer). Furthermore, forced activation of NKT cells with A-GalCer during the secondary immune response in suboptimally immunized animals enhanced otherwise poor tumor rejection responses. Taken together, our findings strongly emphasize the importance of NKT cells in secondary CD8+ T-cell immune responses. [Cancer Res 2009;69(10):4301-8]

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“…Kaplan-Meier survival curve analysis showed that the survival of J␣18 Ϫ/Ϫ mice was statistically significant when compared with survival of wild-type mice ( p ϭ 0.0120), but the survival of CD1d Ϫ/Ϫ mice was not ( p ϭ 0.6038). A dichotomy in the results obtained comparing J␣18 Ϫ/Ϫ and CD1d Ϫ/Ϫ mice has been interpreted in other experimental systems as reflecting a difference between the effects of lacking only V␣14i NKT cells (J␣18 Ϫ/Ϫ mice), and the additional effects of lacking other CD1d-restricted T cells with more diverse TCRs, sometimes called type II NKT cells, in the CD1d Ϫ/Ϫ mice (25,26). In several experimental systems, such as the recurrence of lymphoma growth (25), these type II NKT cells have been shown to have functional capabilities different from V␣14i NKT cells.…”

Section: Reduced Innate Immune Response In Mice Lacking V␣14i Nkt Cellsmentioning

confidence: 99%

Invariant NKT Cells Amplify the Innate Immune Response to Lipopolysaccharide

Nagarajan

Kronenberg²

2007

The Journal of Immunology

249

262

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NKT cells are thought of as a bridge between innate and adaptive immunity. In this study, we demonstrate that mouse NKT cells are activated in response to Escherichia coli LPS, and produce IFN-γ, but not IL-4, although activation through their TCR typically induces both IL-4 and IFN-γ production. IFN-γ production by NKT cells is dependent on LPS-induced IL-12 and IL-18 from APC. LPS induced IFN-γ production by NKT cells does not require CD1d-mediated presentation of an endogenous Ag and exposure to a combination of IL-12 and IL-18 is sufficient to activate them. In mice that are deficient for NKT cells, innate immune cells are activated less efficiently in response to LPS, resulting in the reduced production of TNF and IFN-γ. We propose that in addition to acting as a bridge to adaptive immunity, NKT cells act as an early amplification step in the innate immune response and that the rapid and complete initiation of this innate response depends on the early production of IFN-γ by NKT cells.

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The Contribution of NKT Cells, NK Cells, and Other γ-Chain-Dependent Non-T Non-B Cells to IL-12-Mediated Rejection of Tumors

Cited by 49 publications

References 25 publications

Isolation of murine hepatic lymphocytes using mechanical dissection for phenotypic and functional analysis of NK1.1⁺cells

Isolation of murine hepatic lymphocytes using mechanical dissection for phenotypic and functional analysis of NK1.1⁺cells

Regulation of Secondary Antigen-Specific CD8+ T-Cell Responses by Natural Killer T Cells

Invariant NKT Cells Amplify the Innate Immune Response to Lipopolysaccharide

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The Contribution of NKT Cells, NK Cells, and Other γ-Chain-Dependent Non-T Non-B Cells to IL-12-Mediated Rejection of Tumors

Cited by 49 publications

References 25 publications

Isolation of murine hepatic lymphocytes using mechanical dissection for phenotypic and functional analysis of NK1.1+cells

Isolation of murine hepatic lymphocytes using mechanical dissection for phenotypic and functional analysis of NK1.1+cells

Regulation of Secondary Antigen-Specific CD8+ T-Cell Responses by Natural Killer T Cells

Invariant NKT Cells Amplify the Innate Immune Response to Lipopolysaccharide

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Product

Resources

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Isolation of murine hepatic lymphocytes using mechanical dissection for phenotypic and functional analysis of NK1.1⁺cells

Isolation of murine hepatic lymphocytes using mechanical dissection for phenotypic and functional analysis of NK1.1⁺cells