Immune Specific Induction of Interferon Production in Cultures of Human Blood Lymphocytes

Green, Jonathan A.; Cooperband, Sidney R.; Kibrick, Sidney

doi:10.1126/science.164.3886.1415

Cited by 272 publications

(81 citation statements)

References 5 publications

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“…A local interferon response, perhaps mediated by sensitized lymphocytes migrating into the skin, may be critical in halting virus replication and thus preventing viremia. That sensitized lymphocytes release interferon in response to nonviral antigens has been shown (27) in vitro, and it has been demonstrated that lymphocytes may be the critical effector cell in interferon production in some ' The differences in V-IF response between patients with localized and disseminated disease may be even greater than suggested here. To obtain serial samples from patients with localized disease we select for patients with larger primary involvement and longer duration of lesions, patients with localized disease likely to be deficient in the parameters under study.…”

Section: Discussioncontrasting

confidence: 43%

Interferon, antibody, and other host factors in herpes zoster

Stevens¹,

Merigan²

1972

J. Clin. Invest.

102

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A B S T R A C T The influence of several factors on the course of herpes zoster was studied in 151 patients. Dissemination of zoster was associated with the presence of a concurrent disease, especially Hodgkin's disease, and/or the use of immunosuppressive therapy. Several host-immune parameters, including quantitative immunoglobulins, circulating lymphocyte counts, delayed hypersensitivity to multiple skin test antigens, and lymphocyte transformation to phytohernagglutinin did not correlate with dissemination of disease. Development of virus-specific complement-fixing antibody (CFA) was delayed in some patients with disseminated disease.Vesicle interferon (V-IF) titers were low early in the disease in patients with localized and disseminated zoster and then rose, usually abruptly, to a peak value and declined as pustulation and crusting occurred. However, titers in patients with localized disease rose at an earlier time. This could be seen in terms of time to development of intermediate values of V-IF or by the day on which the sharpest rise occurred. In 15 carefully studied patients with disseminated disease, the development of the maximum V-IF response was followed within 48 hr by cessation of dissemination. Half of the patients in this group had no CFA detectable until after dissemination had ceased.These findings suggest at least two host factors whose interaction might determine host response to zoster; local interferon production (possibly mediated by sensitized lymphocytes) and humoral antibody, acting to prevent or shorten dissemination of an initially local disease.

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Section: Discussioncontrasting

confidence: 43%

Interferon, antibody, and other host factors in herpes zoster

Stevens¹,

Merigan²

1972

J. Clin. Invest.

102

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“…Brunner and his coworkers (19) found that prior treatment of sensitized lymphocytes with specific soluble antigen increased their cytotoxicity. It is of interest that contact between specific antigen and sensitized lymphocytes or target cell and sensitized lymphocytes induces a rapid release of interferon (23,24). It is thus possible that the enhancement of cytotoxicity observed by Brunner et al (19) was in fact mediated by interferon.…”

Section: Specificity Of the Interferon-mediated Enhancement Of Cytotomentioning

confidence: 99%

Enhancement by Interferon of the Specific Cytotoxicity of Sensitized Lymphocytes

Lindahl¹,

Leary²,

Gresser³

1972

Proc. Natl. Acad. Sci. U.S.A.

270

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Mouse interferon preparations enhanced the specific cytotoxicity of sensitized lymphocytes for allogeneic target tumor cells. The factor responsible for the enhancement of cytotoxicity could not be dissociated from the antiviral activity of interferon by standard physicochemical means. Thus, in addition to its well-known antiviral activity, and its effect on cell division, interferon also appears to enhance a specialized cellular function. It is suggested that a common mechanism of action underlies these seemingly different biologic phenomena, and that interferon may play a role in the regulation of fundamental cellular processes.In addition to its well-known antiviral activity, interferon has been shown to inhibit the multiplication of tumor and normal'mammalian cells in culture (1-4). It seems likely, therefore, that the antiviral action of interferon is only one expression of the effect of interferon on cells (3, 4). In the course of our studies on interferon-cell interactions, we observed that prior treatment of sensitized splenic lymphocytes with interferon resulted in an enhancement of the specific cytotoxicity of these cells for target tumor cells. Thus, interferon appears to enhance a specialized cellular function. The results of these experiments and the evidence suggesting that interferon was the factor responsible for enhancement of cytotoxicity of sensitized lymphocytes for target tumor cells are presented herein. MATERIALS AND METHODSImmunization of Mice with L 1210 Cells. Mouse lymphoid leukemia L 1210 cells (5) were maintained by serial passage in ascitic form in DBA/2 mice. For immunization, C 57 BL/6 mice were injected intraperitoneally with 5 X 107 L 1210 cells. The spleens of immunized mice were usually harvested 10 days after injection.Lymphocytes. Suspensions of splenic lymphocytes from immunized or normal C 57 BL/6 mice were obtained according to the method of Brunner et al. (6). The washed lymphocytes were suspended in Eagle's medium containing 10% heatinactivated calf serum -at a density of 20 X 106 viable' cells per ml.Target Cells. L 1210 cells, an interferon resistant subline of L 1210 cells (7) (L 1210-R) and Ehrlich ascites cells (7) were grown in nonagitated suspension cultures in nutrient medium RPMI 1640 (Gibco), supplemented with 10% heatAbbreviation: NDV, Newcastle Disease Virus. 721 inactivated horse serum, 1% iL-glutamine (10 mM/ml), penicillin (200 U/ml), and streptomycin (40 pg/ml). For labeling with radioactive chromium (51Cr), 1 ml of a cell suspension (5 X 106 viable cells per ml) was incubated for 30 min at 37°with 0.1 ml of Na251CrO4 (200 uCi/ml, specific activity 400 mCi/mg of chromium, Centre d'Energie Atomique, France), according to the method of Brunner et al. (6,8). The cell suspensions were washed three times and readjusted to a density of 2 X 106 viable cells per ml.Interferon and Control Preparations. Mouse interferon preparations were obtained from the nutrient medium of monolayer cultures of MSV-Ia (9), L-929 (10), and L cells (11,12) that were inocula...

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“…The synthesis of interferon from lymphocytes can also be induced by immune stimulation (bacterial [16] and viral antigens [17][18][19], alloantigens [20]), anti-lymphocyte sera (21), and mitogenic lectins (22).…”

mentioning

confidence: 99%

Anti-viral activity induced by culturing lymphocytes with tumor-derived or virus-transformed cells. Identification of the anti-viral activity as interferon and characterization of the human effector lymphocyte subpopulation.

Trinchieri¹,

Santoli²,

Dee³

et al. 1978

The Journal of Experimental Medicine

265

102

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A viral inhibitor(s) is released in the supernate of mixed cultures containing human or mouse lymphocytes and cells from certain lines. The inhibitor is active against a variety of unrelated viruses and is a protein that is not toxic for cells. It does not inactivate viruses directly, but inhibits viral replication through an intracellular mechanism that involves synthesis by the cells of both RNA and protein. These characteristics identify the inhibitor as an interferon. The anti-viral activity is contained in at least two molecular species, of approximately 25,000 and 45,000 daltons, respectively. In addition to the anti-viral activity, the supernates of the mixed cultures display an anti-cellular activity, the inhibition of DNA synthesis and of cell multiplication. The anti-viral and the anti-cellular activities are positively correlated in supernates from various cultures and in partially purified preparations. The human cell population responsible for interferon production is composed mainly of Fc-receptor positive, surface immunoglobulin negative, non-T-cell lymphocytes. The ability of certain cell lines to induce interferon seems to be preferentially associated with tumor origin or with in vitro transformation by certain viruses (Epstein-Barr virus, murine sarcoma virus).

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Immune Specific Induction of Interferon Production in Cultures of Human Blood Lymphocytes

Cited by 272 publications

References 5 publications

Interferon, antibody, and other host factors in herpes zoster

Interferon, antibody, and other host factors in herpes zoster

Enhancement by Interferon of the Specific Cytotoxicity of Sensitized Lymphocytes

Anti-viral activity induced by culturing lymphocytes with tumor-derived or virus-transformed cells. Identification of the anti-viral activity as interferon and characterization of the human effector lymphocyte subpopulation.

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