Long term culture of tumour-specific cytotoxic T cells

Gillis, Steven; Smith, Kendall A.

doi:10.1038/268154a0

Cited by 1,300 publications

(531 citation statements)

References 7 publications

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“…The IL-2-dependent mouse T-cell line CTLL-2 20 was maintained in RPMI 1640 medium with 10% heat-inactivated FBS (JRH Biosciences, Lenexa, KS), 1 nM 2-mercaptoethanol and 1 nM recombinant human IL-2 (Takeda Chemical Industries, Osaka, Japan). The IL-2-dependent human T-cell line Kit 225 21 was maintained in RPMI 1640 medium containing 10% FBS and 1 nM IL-2.…”

Section: Cell Lines and Reagentsmentioning

confidence: 99%

Transcriptional activation of survivin through the NF‐κB pathway by human T‐cell leukemia virus type I tax

Kawakami

Tomita

Matsuda

et al. 2005

Intl Journal of Cancer

142

112

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Survivin, a unique member of the inhibitor of apoptosis protein family, is overexpressed in many cancers and considered to play an important role in oncogenesis. We previously reported the survivin expression profile in ATL, a CD4-positive T-cell malignancy caused by HTLV-I. HTLV-I Tax is thought to play an important role in immortalization of T cells. We have shown also that the expression of Tax protected the mouse T-cell line CTLL-2 against apoptosis induced by deprivation of IL-2 and converted its growth from being IL-2 dependent to being IL-2 independent through the NF-kB pathway. In our study, we demonstrate that constitutive expression of survivin was associated with resistance to apoptosis after IL-2 deprivation in Tax-expressing CTLL-2 cells. Transient transfection assays showed that survivin promoter was transactivated by Tax, via the activation of NF-kB. Pharmacological NFkB inhibition resulted in suppression of survivin expression and caused apoptosis of Tax-expressing CTLL-2 cells. Our findings suggest that activated NF-kB signaling contributes directly to malignant progression of ATL by preventing apoptosis, acting through the prosurvival protein survivin. ' 2005 Wiley-Liss, Inc.

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Section: Cell Lines and Reagentsmentioning

confidence: 99%

Transcriptional activation of survivin through the NF‐κB pathway by human T‐cell leukemia virus type I tax

Kawakami

Tomita

Matsuda

et al. 2005

Intl Journal of Cancer

142

112

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“…When 18.5 kBq 3 H-TdR 24 h before harvest. 17 Data shown are the 1 × 10 6 or 1 × 10 7 splenic T cells were transferred with mean of triple cultures.…”

Section: Ctll-2 (Il-2) or Ct4s (Il-4) Assay Influences Of Host Ag Onmentioning

confidence: 99%

Effects of non-major histocompatibility antigens on acute graft-versus-host reaction after allogeneic bone marrow transplantation

Takahashi

Nishihori

Matsuki

et al. 1997

Bone Marrow Transplant

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Summary:the GVHR preventing recurrence of leukemia, via a graftversus-leukemia (GVL) effect.In the present study, using experimental BMT in a mouse In the present study using an experimental BMT system we analyzed the effects of disparity at non-MHC Ag system we investigated the influence of mismatch at non-MHC loci on acute GVHR. We focused particularly on including minor lymphocyte stimulatory-1 a (Mls-1 a ) Ag on the acute GVH reaction (GVHR) induced by MHC minor lymphocyte stimulatory (Mls)-1 a Ags expressed on host tissue. The Mls-1 a Ag is an endogenous superantigen class I Ag. Mismatch at MHC (class I) Ag alone did not induce clinically detectable acute GVHR in this model.and stimulates several repertoires of T cells in the absence of priming. 8,9 It seemed that mismatch at the Mls-1 locus However, BMT mice prepared with a combination of both class I and non-MHC Ag mismatches showed signs between donors and recipients resulted in significant modification of acute GVHR. [10][11][12][13][14][15][16] We report different immunoof clinical GVHR and various cytokines were produced by the spleen cells at an early stage (4 days) after BMT.logical characteristics seen among donor T cells from various BMT chimeras where MHC and/or minor Ag are Although no clinical GVHR was detected in BMT chimeras prepared with a non-MHC mismatched but MHC matched or mismatched. The Mls-1 disparity significantly modified T cell responses and augmented or altered the matched combination, large amounts of various cytokines were secreted by spleen cells. Cytokine production GVHR generated against MHC via elevated cytokine production. in the latter two kinds of chimeras paralleled the increase of Mls-1 a reactive V␤6 ؉ T cells in the host spleen. Marked cytokine production induced by Mls-1 a Materials and methods Ag was confirmed by MLR. Thus, these cytokines appeared to be produced by T cells responding to MlsMice 1 a (ie V␤6 ؉ T cells) and to augment the T cell responses to MHC class I which resulted in clinically detectable B10.AQR (K q A k E k D d , Thy1.2, Mls-1 b ) mice were main-GVHR in chimeras prepared with the combination mistained in our animal facility at Hokkaido University. AKR/J matched at both MHC class I and non-MHC loci.(AKR) (K k A k E k D k , Thy1.1, Mls-1 a ) mice were obtained

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“…It was interesting to note that lymphocytes of one patient, sensitized in vitro in a 3-cell assay, could kill target autochthon- (Zarling & Bach, 1979;Wagner, 1978), helper factor produced by mitogen-activated lymphocytes for maintenance of cytotoxic cells in vitro (Gills & Smith, 1977) or addition of interferon in the stimulating system (Zarling & Bach, 1979). Using animal models, it has also been possible to prevent tumour growth by mixing tumour cells with CTL generated in vitro (Glaser, 1979).…”

Section: Discussionmentioning

confidence: 99%

“…Using animal models, it has also been possible to prevent tumour growth by mixing tumour cells with CTL generated in vitro (Glaser, 1979). Recent evidence suggest that it is possible to maintain specific cytotoxic T cells in vitro by repetitive MLC stimulus and mitogeninduced growth factor for 4 months (Gills & Smith, 1977;Zarling & Bach, 1979). The system thus has great potential and applicability in human situations.…”

Section: Discussionmentioning

confidence: 99%

In vitro generation of lymphocytotoxicity to autochthonous leukaemic cells in chronic myeloid leukaemia

Khare¹,

Advani²,

Gangal³

1981

Br J Cancer

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Summary.-Lymphocytes from 13 chronic myeloid leukaemia (CML) patients in remission were tested for their ability to differentiate in vitro into a cell population cytotoxic to autochthonous target leukaemic cells. CML remission lymphocytes were cultured in vitro with autochthonous leukaemic cells and allogeneic normal lymphocytes from an unrelated donor, singly or in combination. The cytotoxic lymphocytes obtained after 7 days of culture were tested for their ability to kill autochthonous leukaemic cells in a 3h 5lCr-release assay. It was found that with the allogeneic stimulus alone, cytotoxicity was generated in 5/13 cases, whilst stimulation of lymphocytes with autochthonous leukaemic cells alone induced cytotoxicity in 7/13 cases. In contrast, anti-leukaemic cytotoxicity was shown in 12/13 cases when responder lymphocytes were stimulated with both autochthonous leukaemic and unrelated allogeneic normal lymphocytes.The specificity of cytotoxicity was confirmed using other targets such as autochthonous PHA-transformed lymphoblasts and mouse L1210 cells. In 1/5 cases, CML remission lymphocytes stimulated with autochthonous leukaemic cells showed cytotoxicity to PHA-transformed autochthonous normal lymphoblasts, whilst 1/4 patients showed nonspecific cytotoxicity to L1210 cells when lymphocytes were cultured in MLC or MLTC, as well as in a 3-cell assay.

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Long term culture of tumour-specific cytotoxic T cells

Cited by 1,300 publications

References 7 publications

Transcriptional activation of survivin through the NF‐κB pathway by human T‐cell leukemia virus type I tax

Transcriptional activation of survivin through the NF‐κB pathway by human T‐cell leukemia virus type I tax

Effects of non-major histocompatibility antigens on acute graft-versus-host reaction after allogeneic bone marrow transplantation

In vitro generation of lymphocytotoxicity to autochthonous leukaemic cells in chronic myeloid leukaemia

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