<i>In Vivo</i>Augmentation of Natural Killer Activity by Combined Treatment with Recombinant Gamma Interferon and Interleukin-2

Shalaby, M. R.; Svedersky, L P; McKay, Patrick; Finkle, Bryan S.; Palladino, Michael A.

doi:10.1089/jir.1985.5.571

Cited by 28 publications

(10 citation statements)

References 27 publications

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“…The collaboration between IL-2 and IFN on NK activity in vivo has been reported. Shalaby et al demonstrated that, compared with animals receiving treatment with either IFN-y or IL-2 alone, the sequential treatment of mice with both agents resulted in a significantly greater enhancement of NK cell activity [35]. Thus the involvement of IFN-7 in the enhancement of NK activity is controversial.…”

Section: Discussionmentioning

confidence: 99%

Role of interleukin-2 and interferon-? in induction of activated natural killer cells from mice primed in vivo and subsequently challenged in vitro with the streptococcal preparation OK432

Yamaue¹,

Tanimura²,

Itō³

et al. 1989

Cancer Immunol Immunother

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The natural-killer(NK)-cell-mediated cytotoxicity to syngeneic tumor cells can be augmented by in vivo priming and subsequent in vitro challenge with the streptococcal preparation OK432. Supernatants of cocultures of spleen cells with OK432 contained interleukin-2 (IL-2) and interferon (IFN), mainly IFN-gamma. As the anti-(mouse IFN-gamma) monoclonal antibody but not anti-(mouse IFN-alpha) antibody inhibited the induction of activated NK cells with OK432, the IFN-gamma participated in this response. The enhancement of NK cell activity and production of IL-2 were partially inhibited by the pretreatment of spleen cells with mitomycin C or irradiation, and were completely abolished by pretreatment with actinomycin D. The IL-2 activity after treatment with various metabolic inhibitors ran parallel to the NK activity in a system augmented with OK432. The activity of incubated spleen cells with IL-2 receptors was increased by OK432 treatment, and the NK cell and IFN activities of supernatants were also abrogated by the treatment with anti-(mouse IL-2 receptor) monoclonal antibody, to block the interaction between IL-2 and these receptors of effector cells. The panning method clarified that the incubated spleen cells with IL-2 receptors are responsible for the production of IFN-gamma. These results suggest that IL-2 plays a major role in inducing the activated NK cells from murine spleen cells primed in vivo and subsequently challenged in vitro with OK432, by the production of IFN-gamma.

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Section: Discussionmentioning

confidence: 99%

Role of interleukin-2 and interferon-? in induction of activated natural killer cells from mice primed in vivo and subsequently challenged in vitro with the streptococcal preparation OK432

Yamaue¹,

Tanimura²,

Itō³

et al. 1989

Cancer Immunol Immunother

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“…To rule out that a significant increase in NK activity was not missed due to the early kinetics of the response, we examined YAC-1 killing in BALB/c mice receiving KBALB-GRP94⌬KDEL cells 0, 2, and 4 days following cell administration, and again we observed no significant increase (data not shown). As an internal control in these experiments, 51 Cr-labeled YAC-1 targets were incubated with splenocytes from naive BALB/c mice stimulated in vitro with 1000 U/ml rIL-2, a potent stimulus for NK activity (28). Under these conditions, a pronounced activation of YAC-1-directed NK function was observed ( Fig.…”

Section: In Vivo Administration Of Grp94/gp96-secreting Fibroblasts Dmentioning

confidence: 99%

Glucose-Regulated Protein 94/Glycoprotein 96 Elicits Bystander Activation of CD4+ T Cell Th1 Cytokine Production In Vivo

Baker-LePain¹,

Sarzotti

Nicchitta³

2004

The Journal of Immunology

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Glucose-regulated protein 94 (GRP94/gp96), the endoplasmic reticulum heat shock protein 90 paralog, elicits both innate and adaptive immune responses. Regarding the former, GRP94/gp96 stimulates APC cytokine expression and dendritic cell maturation. The adaptive component of GRP94/gp96 function reflects a proposed peptide-binding activity and, consequently, a role for native GRP94/gp96-peptide complexes in cross-presentation. It is by this mechanism that tumor-derived GRP94/gp96 is thought to suppress tumor growth and metastasis. Recent data have demonstrated that GRP94/gp96-elicited innate immune responses can be sufficient to suppress tumor growth and metastasis. However, the immunological processes activated in response to tumor Ag-negative sources of GRP94/gp96 are currently unknown. We have examined the in vivo immunological response to nontumor sources of GRP94/gp96 and report that administration of syngeneic GRP94/gp96- or GRP94/gp96-N-terminal domain-secreting KBALB fibroblasts to BALB/c mice stimulates CD11b+ and CD11c+ APC function and promotes bystander activation of CD4+ T cell Th1 cytokine production. Only modest activation of CD8+ T cell or NK cell cytolytic function was observed. The GRP94/gp96-dependent induction of CD4+ T cell cytokine production was markedly inhibited by carrageenan, indicating an essential role for APC in this response. These results identify the bystander activation of CD4+ T lymphocytes as a previously unappreciated immunological consequence of GRP94/gp96 administration and demonstrate that GRP94/gp96-elicited alterations in the in vivo cytokine environment influence the development of CD4+ T cell effector functions, independently of its proposed function as a peptide chaperone.

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“…TNF, like IFN, increases the expression of HLA-A, B antigens (38) suggesting that TNF may enhance the participation of cytolytic T lymphocytes in the destruction of neoplastic or virally-altered cells. In addition, TNF in vitro stimulates an increase in the phagocytic abilities of polymorphonuclear cells (10), cells which are capable of virus particle inactivation and tumor cell destruction (39,40). Recently, TNF was shown to protect 'aged" human fibroblasts from the cytopathic effect of encephalomyocarditis virus (41 …”

Section: D-i-s-czs ¶Io1mentioning

confidence: 99%

“…In addition to the historically studied cytotoxicity toward neoplastic tissue, a broad spectrum of activity has now been attributed to this molecule. TNF can participate in the inflammatory response by altering host metabolism and thereby mediating cachexia (9), activating polymorphonuclear neutrophil phagocytic and cytotoxic functions (10), enhancing eosinophil toxicity (11), and modulating the procoagulant properties of Nucleic Acids Research vascular endothelial cells (12,13). TNF can also stimulate bone resorption (14) and fibroblast growth (15).…”

Section: Introductiqmentioning

confidence: 99%

Sendai virus induces high levels of tumor necrosis factor mRNA in human peripheral blood leukocytes

Berent¹,

Torczynski²,

Bollon³

1986

Nucl Acids Res

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ABSTRACSendai virus induces human peripheral blood leukocytes to produce high levels of tumor necrosis factor (TNF) mRNA. TNF mRNA can represent as much as 0.6% of the total mRNA. Kinetic studies indicate that the level of TNF mRNA peaks about 2 hours before that of IFN-a mRNA produced in the same system. Although the peak levels of TNF and IFN-a mRNA were similar, TNF in the culture supernatants was at a 200 fold lower level than IFN--. Cloning and sequence analysis of TNF cDNA isolated from peripheral blood leukocytes RNA showed that normal human cells in response to Sendai virus produce TNF identical to that previously isolated and cloned from tumor-derived cell lines. A bacterial expression system was used to produce the cloned TNF at a maximum level of 2 X 106 units per ml of culture.

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In VivoAugmentation of Natural Killer Activity by Combined Treatment with Recombinant Gamma Interferon and Interleukin-2

Cited by 28 publications

References 27 publications

Role of interleukin-2 and interferon-? in induction of activated natural killer cells from mice primed in vivo and subsequently challenged in vitro with the streptococcal preparation OK432

Role of interleukin-2 and interferon-? in induction of activated natural killer cells from mice primed in vivo and subsequently challenged in vitro with the streptococcal preparation OK432

Glucose-Regulated Protein 94/Glycoprotein 96 Elicits Bystander Activation of CD4+ T Cell Th1 Cytokine Production In Vivo

Sendai virus induces high levels of tumor necrosis factor mRNA in human peripheral blood leukocytes

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