Immunization with MHC class I-negative but not -positive HPV16-associated tumour cells inhibits growth of MHC class I-negative tumours

Reiniš, Milan; Šímová, Jana; Indrová, M; Bieblová, Jana; Přibylová, Hana; Moravcová, Simona; Jandlová, T; Bubenı́k, Jan

doi:10.3892/ijo.30.4.1011

Cited by 8 publications

(14 citation statements)

References 32 publications

(37 reference statements)

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“…In this communication, our previously obtained results (14,15) Collectively, our results indicate an important role of NK1.1 + cells and IFNÁ production by these cells in the induction of the protective immunity against MHC I-deficient HPV16-associated tumours. NK1.1 + cells seem to be an important part of the complex mechanism in development of specific immunity against MHC class I-deficient tumours that includes the cooperation of various cell subsets.…”

Section: Discussionmentioning

confidence: 66%

“…In our previous studies, it was found that immunization with cellular vaccines based on MHC class I-deficient tumour cells was effective against MHC class I-deficient tumours, as well as against their 'parental' MHC class I-positive tumours, due to the antigen cross-presentation (14). Moreover, we have shown, using the same model, that immunization with peptides, peptide-pulsed DC or MHC class I-deficient tumour cells can elicit specific immunity against these tumours, but the MHC class I expression status has to be considered in optimization of the vaccination strategy (15).…”

Section: Discussionmentioning

confidence: 99%

“…In vivo depletion studies in the course of the tumour growth revealed that the effective immune responses against MHC class I-negative tumours in animals immunized with MHC class I-deficient tumour cells were dependent on natural killer cells. Using the same model, we have shown that induction of the specific immunity by immunization with a peptide comprising CTL and Th epitope but not solely a CTL epitope, can elicit protective immunity against MHC class I-deficient tumours (14,15).…”

Section: Introductionmentioning

confidence: 99%

“…The role of indirectly activated CD8 + and CD4 + cells cannot be excluded either (10-13). The data from our previous experiments have shown that immunization with MHC class I-deficient but not with MHC class I-positive tumour cells inhibited the growth of MHC class I-deficient, HPV16-associated murine tumours expressing E6 and E7 viral oncoproteins (14). In vivo depletion studies in the course of the tumour growth revealed that the effective immune responses against MHC class I-negative tumours in animals immunized with MHC class I-deficient tumour cells were dependent on natural killer cells.…”

Section: Introductionmentioning

confidence: 99%

“…In vivo depletion of NK1.1 + , CD4 + and CD8 + cells was performed using monoclonal antibodies PK 136 (anti-NK1.1 + ), GK 1.5 (anti-CD4 + ), and 2.43 (anti-CD8 + ), respectively, for 4 weeks, starting day -37 (14,(20)(21)(22)(23)(24)(25). To deplete the effector cells, 0.1 mg of the antibody was injected i.p.…”

Section: Introductionmentioning

confidence: 99%

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NK1.1+ cells are important for the development of protective immunity against MHC I-deficient, HPV16-associated tumours

Indrová

Šímová²,

Bieblová³

et al. 2010

Oncol Rep

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Section: Discussionmentioning

confidence: 66%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

NK1.1+ cells are important for the development of protective immunity against MHC I-deficient, HPV16-associated tumours

Indrová

Šímová²,

Bieblová³

et al. 2010

Oncol Rep

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Therapy for minimal residual tumor disease: β‐Galactosylceramide inhibits the growth of recurrent HPV16‐associated neoplasms after surgery and chemotherapy

Šímová

Indrová

Bieblová

et al. 2010

Intl Journal of Cancer

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Natural killer T (NKT) cells are potent modulators of antitumor immunity. Their protective effects can be achieved upon their activation by glycolipid ligands presented in the context of the CD1d molecule. These CD1d-binding glycolipid antigens have been described as potent therapeutic agents against tumors, infections, as well as autoimmune diseases. Immunoregulatory and therapeutic effects of glycolipid ligands depend on their structure and modes of administration. Therefore, more studies are needed for optimization of the particular therapeutic settings. This study was focused on the tumor-inhibitory effects of 12 carbon acyl chain b-galactosyl ceramide (C12 b-D-Galactosyl Ceramide; b-GalCer(C12)) on the growth of human papillomavirus type 16 (HPV16)-associated neoplasms transplanted in syngeneic mice. Treatment of tumor-bearing mice with b-GalCer(C12) 3-14 days after tumor cell transplantation significantly inhibited the growth of the major histocompatability complex (MHC) Class I-positive (TC-1), as well as MHC Class I-deficient (TC-1/A9) HPV16-asssociated tumors. Moreover, administration of b-GalCer(C12) after surgical removal of TC-1 tumors inhibited the growth of tumor recurrences. Similar results were obtained in the treatment of tumors after chemotherapy. b-GalCer(C12) treatment turned out to be also synergistic with immunotherapy based on administration of IL-12-producing cellular vaccines. These results suggest that bGalCer(C12), whose antitumor effects have so far not been studied in detail, can be effective for the treatment of minimal residual tumor disease as well as an adjuvant for cancer immunotherapy.Natural killer T (NKT) cells characterized by cell surface expression of T-cell and NK-cell receptors are important immune regulators that can either promote or suppress antitumor and anti-infection immunity, as well as autoimmunity.1-3 Antitumor activities of NKT cells have mainly been attributed to their Type I (expressing Va14Ja18 and Va24Ja18 TCRa in mice and humans, respectively) that recognize glycolipid antigens in the context of major histocompatability complex (MHC) Class I-like molecule CD1d. NKT cells can be modulated by analogues of their natural, so far poorly characterized, glycolipid ligands. Their specific effects, e.g. induction of cytokine production, NKT cell expansion and activation of a variety of immune cells, as well as NKT cell receptor downregulation and induction of NKT cell anergy strongly depend on their structure and mode of administration. 4,5 So far, most in vivo studies investigating antitumor potential of NKT cell-activating glycolipids have been focused on a-galactosylceramide, originally described as an antitumor drug.6 Much less is known about the antitumor effects of b-anomers. Several clinical studies were performed in which the patients were given either free a-galactosylceramide (a-GalCer) or dendritic cells pulsed with a-GalCer.7-9 In these trials, NKT cell activation/expansion and cytokine production was observed in the treated patients. However, the immun...

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The Natural Killer Cell Cytotoxic Function Is Modulated by HIV-1 Accessory Proteins

Sowrirajan

Barker

2011

Viruses

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Natural killer (NK) cells’ major role in the control of viruses is to eliminate established infected cells. The capacity of NK cells to kill virus-infected cells is dependent on the interactions between ligands on the infected cell and receptors on the NK cell surface. Because of the importance of ligand-receptor interactions in modulating the NK cell cytotoxic response, HIV has developed strategies to regulate various NK cell ligands making the infected cell surprisingly refractory to NK cell lysis. This is perplexing because the HIV-1 accessory protein Vpr induces expression of ligands for the NK cell activating receptor, NKG2D. In addition, the accessory protein Nef removes the inhibitory ligands HLA-A and -B. The reason for the ineffective killing by NK cells despite the strong potential to eliminate infected cells is due to HIV-1 Vpu’s ability to down modulate the co-activation ligand, NTB-A, from the cell surface. Down modulation of NTB-A prevents efficient NK cell degranulation. This review will focus on the mechanisms through which the HIV-1 accessory proteins modulate their respective ligands, and its implication for NK cell killing of HIV-infected cells.

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Immunization with MHC class I-negative but not -positive HPV16-associated tumour cells inhibits growth of MHC class I-negative tumours

Cited by 8 publications

References 32 publications

NK1.1+ cells are important for the development of protective immunity against MHC I-deficient, HPV16-associated tumours

NK1.1+ cells are important for the development of protective immunity against MHC I-deficient, HPV16-associated tumours

Therapy for minimal residual tumor disease: β‐Galactosylceramide inhibits the growth of recurrent HPV16‐associated neoplasms after surgery and chemotherapy

The Natural Killer Cell Cytotoxic Function Is Modulated by HIV-1 Accessory Proteins

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