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At least 1,387 records · Page 77Linked to original sources
PubMed1992

Interferon-alpha 2b instillation prophylaxis in superficial bladder cancer--a prospective, controlled three-armed trial. Project Group Bochum--Interferon and Superficial Bladder Cancer.

Sixty-seven patients with recurrent pTa G1-G3 to pT1 G1-G3 tumors were randomized into three groups receiving either Intron A at 10 MU/instillation, Intron A at 10 MU and mitomycin C (MMC) at 20 mg/instillation or MMC at 20 mg/instillation. After a mean follow up of 6.2 months no tumor recurrence has been seen in the group receiving combined therapy, whilst four out of 22 in the interferon group and five out of 23 in the MMC group suffered a recurrence. Side effects were slight. These preliminary results suggest that a combination of the two drugs is more effective than either drug alone.

Aged↗
PubMed1992

The antagonistic effect of interferon-beta on the interferon-gamma-induced expression of HLA-DR antigen in a squamous cell carcinoma line.

We examined the effect of type I interferon (IFN) on IFN-gamma-induced HLA-DR antigen expression in A431 cells, a human squamous cell carcinoma line. A431 cells expressed HLA-DR antigen when stimulated with IFN-gamma, but not with IFN-beta. Simultaneous addition of IFN-gamma and IFN-beta to A431 cells resulted in significantly decreased HLA-DR antigen expression when compared to treatment with IFN-gamma alone. Kinetic studies revealed that IFN-beta was required concomitantly or prior to stimulation with IFN-gamma in order to down-regulate expression of HLA-DR antigens. IFN-alpha also inhibited IFN-gamma-induced HLA-DR antigen expression in A431 cells. Analysis of cytoplasmic mRNA showed that simultaneous treatment of A431 cells with IFN-gamma and IFN-beta resulted in a marked decrease of the level of DR alpha specific mRNA when compared to a level reached after treatment with IFN-gamma alone. These results suggest that type I IFN antagonize the IFN-gamma-induced HLA-DR antigen expression in human keratinocyte system, and that this antagonistic effect of type I IFN is confirmed as evidenced by a change in HLA-DR mRNA levels.

Blotting, Northern↗
PubMedDate not supplied

Comparison of lamivudine and alpha-interferon combination with alpha-interferon alone in the treatment of HBeAg-positive chronic hepatitis B.

AIM: To compare the efficacy of a combination of a-interferon (IFN-a) and lamivudine with IFN-a alone in the treatment of patients with HBeAg-positive chronic hepatitis B (CHB). METHODS: Sixty-eight treatment-naove patients with HBeAg-positive CHB were randomized to receive either 9 MU of IFN-a2a three times a week and lamivudine 100 mg daily (Group 1), or IFN-a2a alone in the same dosage (Group 2), for 12 months. Serum ALT, HBeAg, anti-HBe and HBV DNA were tested at the end of treatment and 6 months later. Complete response was defined as normal ALT, negative HBeAg and negative HBV DNA, six months after stopping treatment. RESULTS: Of the 68 patients, 64 completed the study. In Group 1 (n=31), mean (SD) ALT levels decreased from 124 (59) IU/L to 39 (18) IU/L at 12 months; corresponding values in Group 2 (n=33) were 128 (57) and 56 (11) IU/L (p< 0.05). Absence of HBV DNA at the end of treatment was more common in Group 1 (28/31) than in Group 2 (22/33; p< 0.022). The number of patients with seroconversion to anti-HBe (4/31 [13%] vs. 4/33 [12%], respectively; p>0.05), as also those with complete response (4/31 [13%] and 4/33 [12%], respectively; p>0.05) six months after completion of treatment was similar in Group 1 and Group 2. CONCLUSION: Combination treatment with IFN-a and lamivudine was better than IFN-a monotherapy in normalization of ALT and clearance of HBV DNA; however, it did not have a better sustained response rate than IFN-a alone.

Adult↗
PubMedDate not supplied

[Interferon-inducing activity of amixin and its effect on the interferon status].

The national preparation amixine induces interferon (IF) production in most of the people who have background values of serum IF. When the initial values of serum IF are high, after administration of amixine they decline to the background ones. A certain group of subjects (approximately 25%) is not sensitive to amixine. The IF content in the blood serum of such subjects does not change before or after administration of amixine. Its use should be limited to 4-5 administrations weekly, because its longer use leads to the exhaustion of the IF system in people.

Adolescent↗
PubMed1990

Interferon and 2',5'-oligo(A) synthetase activities in serum and blood mononuclear leukocytes of cattle after injection of bovine interferon-alpha 1.

Cell extracts that were prepared from blood mononuclear leukocytes from 66 samples obtained from 6 clinically normal calves contained mean 2',5'-oligoadenylate (2',5'-oligo[A]) synthetase activity sufficient to synthesize 186 +/- 82 pmol of 2',5'-oligo(A)/h/10(6) cells. Calves had no measurable serum interferon (IFN) activity. Five calves were given IM injections of 10(4), 10(5), 5 x 10(5), 10(6), and 10(7) U of bovine IFN-alpha 1/kg of body weight at 2-week intervals. Five dosing sequences were used with a 5 x 5 Latin square design so that each calf received each dose once. Activity of 2',5'-oligo(A) synthetase increased at 24 hours in response to all dosages of IFN and then declined following first-order kinetics, with an apparent half-life (t1/2) of 2.1 +/- 0.5 days. The area under the concentration-time curve for 2',5'-oligo(A) synthetase increased with dose of IFN more rapidly than did peak response. Serum IFN that was measured at 1-day intervals following administration of IFN was consistently measurable only at dosages above 10(6) U of IFN/kg. The t1/2 for circulating IFN was 12.4 +/- 1.0 hours. Over all dosages, increases in 2',5'-oligo(A) synthetase activity were measurable for 3.5 days longer than were increases in IFN following IM injection of IFN. None of the calves developed detectable anti-IFN antibodies.

2',5'-Oligoadenylate Synthetase↗
PubMed2006

[Cloning, prokaryotic expression of chicken interferon-alpha gene and study on antiviral effect of recombinant chicken interferon-alpha].

The full length of chicken interferon alpha (ChIFN-alpha) gene was amplified by the polymerase chain reaction (PCR) from total liver genome of Sanhuang meat-chicken and sequenced. The amplified gene was about 582bp. The coding region for mature protein (489bp) was subcloned into pET-28a(+). The recombinant plasmid pET-28a(+)-IFNalpha was identified by enzyme digestion and DNA sequencing. Data of SDS-PAGE and Western-blot indicated that a 22kD fusion protein was expressed in the form of inclusion bodies with good immunity. The purity of inclusion bodies was above 70% and that of protein purified by nickel affinity chromatography was 95%. The recombinant protein could inhibit H9N2 avian influenza virus (H9N2 AIV) replication on chick embryo fibroblast. 2 microg of recombinant IFN-alpha could completely protect Chick embryo from H9N2 AIV infection. The recombinant IFN-alpha can also delay Newcastle disease virus (NDV) replication on chick embryo for 12 approximately 48h. Chicken administered recombinant IFN-alpha can resist the H9N2 AIV infection. The bioactivities of recombinant IFN-alpha purified by affinity chromatograph were 20 times higher than that of inclusion bodies.

Animals↗
PubMed1991

Loss of interferon antibodies during prolonged continuous interferon-alpha 2a therapy in hairy cell leukemia.

Although highly active in hairy cell leukemia (HCL), interferons (IFN) are not curative in this disease; current data indicate that prolonged IFN therapy will be necessary to control disease in the majority of patients. We previously observed acquired IFN resistance in association with neutralizing IFN-alpha 2a antibodies in small numbers of patients with HCL. This finding suggests that the requisite long-term therapy may be compromised if there is an increasing incidence over time of neutralizing antibodies. We performed a follow-up study of IFN antibodies in our patients receiving continuous IFN therapy. All 16 patients who were previously antibody negative remained so. Surprisingly, all nine patients who previously had non-neutralizing IFN antibodies became antibody negative after a median of 14.5 months. Moreover, 3 of 10 patients who had neutralizing antibodies became antibody negative and five had only non-neutralizing antibodies a median of 10 months from the time neutralizing antibody had first been detected. Only two patients had persisting neutralizing antibodies. Inhibition of neopterin synthesis, inhibition of generation of 2', 5' oligoadenylate synthetase activity, and inability to detect IFN in serum after subcutaneous injection of IFN-alpha 2a was observed only in the one patient tested with neutralizing IFN antibodies confirming that these antibodies have functional significance in vivo. We conclude that, although neutralizing IFN antibodies inhibit the effectiveness of IFN in vivo, these antibodies are produced only transiently during long-term therapy. The long-term effectiveness of this drug will not likely be affected in most patients by neutralizing antibody.

Antibodies↗
PubMed2006

The up-regulation of type I interferon receptor gene plays a key role in hepatocellular carcinoma cells in the synergistic antiproliferative effect by 5-fluorouracil and interferon-alpha.

Combination therapy with interferon (IFN)-alpha and 5-fluorouracil (5-FU) has been reported to show an improved therapeutic efficacy in patients with advanced hepatocellular carcinoma (HCC) but the mechanism behind this has not been completely elucidated. We examined the molecular events underlying the antiproliferative effects of IFN-alpha and 5-FU in combination using six human HCC cell lines. When the antiproliferative effects of administering IFN-alpha and 5-FU together were analyzed using isobolograms, we found that the cell lines could be divided into two groups: the S-group containing three cell lines, which showed synergistic effects, and the A-group, containing the remaining three cell lines, which showed additive effects. Real-time RT-PCR and Western blot analyses revealed that the expression levels of type I IFN receptor subunits, IFNAR1 and IFNAR2, were specifically up-regulated by 5-FU in all three cell lines of the S-group with the exception of IFNAR2 in one cell line, but not in those of the A-group. IFN-alpha modulated the protein expression levels of six enzymes regulating sensitivity to 5-FU, but none of them were down- or up-regulated in the same way in all members of the S- or A-group. In conclusion, the 5-FU-induced modulation of IFN receptor expression could play a pivotal role in the therapeutic efficacy of IFN-alpha combined with 5-FU. Measuring the expression levels of IFN receptors, and their ability to be up-regulated, may be a promising method for selecting HCC patients for this type of combination therapy.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1990

Antitumor effects of alpha-interferon and gamma-interferon on a murine renal cancer (Renca) in vitro and in vivo.

Previous studies have shown that established murine renal cancer (Renca) can be successfully treated with the investigational drug flavone acetic acid (FAA) used in combination with recombinant interleukin 2 (IL-2). Additional experiments demonstrated that the in vivo administration of FAA rapidly induced the expression of the genes, as well as the biologically active proteins, for alpha- and beta-interferons (IFNs) as well as tumor necrosis factor alpha. Both IFN-alpha and IFN-gamma have been shown to have direct antiproliferative effects against some tumors, as well as being potent immunodulators for the induction of antitumor effector cells. Thus, the present study was designed to investigate the ability of IFN-alpha and/or IFN-gamma to mediate direct antiproliferative effects against Renca in vitro as well as to cause regression of Renca in vivo. The present study confirms that RAA and/or IL-2 are inactive against Renca in vitro, further suggesting an indirect mechanism for FAA-induced antitumor effects in vivo. However, the exposure of Renca in vitro to recombinant human IFN-alpha A/D, murine IFN-alpha or murine IFN-beta resulted in a dose dependent growth inhibition of Renca as assessed by the microculture tetrazolium dye incorporation assay. Very little growth inhibition was induced by recombinant murine IFN-gamma. Interestingly, IFN-alpha (100-1000 units/ml) when combined with very low doses of recombinant murine IFN-gamma (1-10 units/ml) yielded significantly more pronounced growth inhibition than either cytokine alone. This effect was most evident by 5 days of culture where combinations of 100-1000 units/ml recombinant human IFN-alpha A/D with 1-5 units/ml recombinant murine IFN-gamma yielded growth inhibition in the range of 45-99%. In order to determine whether the mechanisms for the antitumor activity of recombinant human IFN-alpha A/D and recombinant murine IFN-gamma was due to their direct antiproliferative effects, we also studied the efficacy of these combinations against i.p. Renca in athymic mice. In contrast to the potent antitumor effects observed in euthymic mice, the combination of IFN-alpha and IFN-gamma only slightly increased mean survival times in athymic mice and no long term survivors were obtained. Subsequent studies demonstrated that most mice (77%) cured of peritoneal Renca by recombinant human IFN-alpha A/D plus recombinant murine IFN-gamma were immune to rechallenge. Therefore the combination of IFN-alpha and IFN-gamma may directly inhibit the growth of Renca, but a major effect of IFNs in vivo must be to contribute to the induction of an anti-Renca immune response.

Adjuvants, Immunologic↗
PubMed1990

The down-regulation of alpha-interferon receptors in human lymphoblastoid cells: relation to cellular responsiveness to the antiproliferative action of alpha-interferon.

Human lymphoblastoid cell lines (Daudi, Daudi subclones, Raji and MOLT-4) were compared for sensitivity to the antiproliferative action of alpha-interferon (IFN-alpha) and down-regulation of IFN-alpha receptors. IFN-sensitive and IFN-resistant cell lines have similar numbers (2-4000/cell) of high affinity (20-75 pM) IFN-alpha receptors. Treatment of IFN-sensitive cells with low concentrations (3-10 pM) of IFN-alpha results in low receptor occupancy and nearly complete (greater than 95%) down-regulation of cell surface IFN-alpha receptors within 5 h. Treatment of resistant cells with higher IFN concentrations (30 pM) only results in partial (approximately 60%) receptor down-regulation that is directly related to receptor occupancy. Receptor-receptor interactions, induced by IFN-alpha binding, may account for the enhanced down-regulation of IFN-alpha receptors in IFN-sensitive cells. Such interactions apparently do not occur in IFN-resistant lymphoblastoid cell lines.

Cell Division↗
PubMed1987

Proliferative response of hairy cells to B cell growth factor (BCGF): in vivo inhibition by interferon-alpha and in vitro effects of interferon-alpha, -beta, and -gamma.

Hairy cell leukemia (HCL) is a pre-plasma B cell tumor which responds to interferon (IFN)-alpha therapy. In vitro, B cell growth factor (BCGF) can induce proliferation of hairy cells. We have investigated the effect of in vitro and in vivo treatments with different recombinant IFN on the capacity of hairy cells to proliferate in response to human BCGF. In vitro treatment of leukemic cells from HCL patients with recombinant IFN-alpha-2 (5/5 cases) or IFN-beta (4/5 cases) resulted in a marked inhibition of the BCGF-dependent response. This suppressive effect was obtained with IFN concentrations of 1000, 100 IU/ml, and even occasionally 10 IU/ml. In contrast, no such inhibition was observed with IFN-gamma, despite the presence of specific IFN-gamma receptors on hairy cells at densities similar to receptors for IFN-alpha/beta. The IFN-alpha-induced suppression of the proliferative response of hairy cells to BCGF was also observed in vivo in two patients within 6-12 hr after administration of single doses of IFN-alpha. When hairy cells were maintained in culture for 1 week, they recovered their capacity to be stimulated by BCGF. This reversion was also shown in vivo in hairy cells isolated 1 week after IFN administration. Since in vivo growth of hairy cells could possibly result from the autocrine secretion of BCGF, we propose that the therapeutic effect of IFN-alpha on HCL may be due in part to an inhibition of such autocrine loop.

2',5'-Oligoadenylate Synthetase↗
PubMedDate not supplied

Essentially pure murine interferon-alpha/beta primes poly rI:rC and Sendai virus-induced interferon production in mice.

Intramuscular (i.m.) injection of mice with 2000 IU/g of essentially pure murine interferon-alpha/beta (MuIFN-alpha/beta) 3 h before the induction of IFN by an intraperitoneal (i.p.) inoculation of 10 haemagglutinating units (HAU) per g Sendai virus or 3 micrograms/g polyriboinosinic and polyribocytidylic acid complex (poly rI:rC) elicited a primed IFN response in both cases. Antiserum to MuIFN-alpha/beta neutralized both the priming and antiviral activities of the IFN preparation used. Comparison of the kinetics of primed and unprimed IFN production by Sendai virus indicated that the early (2-4 h) period of IFN production was affected.

Animals↗
PubMed1986

Treatment of hairy cell leukemia with recombinant alpha interferon: II. In vivo down-regulation of alpha interferon receptors on tumor cells.

Interferons (IFNs) initiate their effects by interacting with specific high-affinity cell surface receptors, but little is known about the physiology of IFN receptor interaction in vivo. Treatment of patients suffering from hairy cell leukemia (HCL) with human recombinant alpha IFN results in significant tumor regression, with clinical improvement in a high percentage of cases. To investigate a possible relevance of binding parameters as response markers, IFN receptor interaction on tumor cells responsive to IFN in vivo was studied. Binding of human alpha 2 IFN to circulating hairy cells was analyzed before and during IFN therapy in ten patients selected on the basis of high numbers of peripheral hairy cells. Binding experiments were carried out on Ficoll-Paque fractionated peripheral cell samples containing a majority of hairy cells. All patients reacted to recombinant alpha IFN treatment with a striking decrease in binding capacity within 12 hours after the first injection. As demonstrated by using a monoclonal antibody able to recognize alpha 2 IFN bound to its receptor, this decreased binding capacity was not due to blocking by circulating IFN but rather to a decrease in receptor number. This receptor "down-regulation" was partially reversible after the first IFN injection. However, upon prolonged IFN therapy, all patients displayed a stable state of decreased receptor expression. Down-regulation of IFN receptors can be regarded as a response marker to IFN treatment. This response marker, however, was not correlated with the clinical response within the first months of IFN therapy.

Animals↗
PubMed1987

Specific residues within an amino-terminal domain of 35 residues of interferon alpha are responsible for recognition of the human interferon alpha cell receptor and for triggering biological effects.

Bovine interferon alpha C (IFN-alpha C) manifest at least 10(5)-fold lower antiviral activity on human cells than on bovine cells (Velan, B., Cohen, S., Grosfeld, H., Leitner, M., and Shafferman, A. (1985) J. Biol. Chem. 260, 5498-5504). By oligonucleotide site-directed mutagenesis within the coding region for the NH2-terminal 44-residue domain of BoIFN-alpha C, we replaced up to 18 residues by the corresponding HuIFN-alpha J1 residues. (HuIFN-alpha J1 is less than 60% homologous in sequence to BoIFN-alpha C.) The nine different bovine-human-IFN alpha hybrids obtained were compared to BoIFN-alpha C and HuIFN-alpha J1 with respect to their potential to induce an antiviral state, synthesis of 2-5A-synthetase, and their specific binding to human and bovine cells. Relative to BoIFN-alpha C, a gradual increase in biological activities (antiviral or 2-5A-synthetase) of approximately 10-, 10(2)-, 10(3)-, and approximately 10(4)-fold is obtained, depending on the number and positions of the residues substituted. A direct correlation exists between biological response and ability of IFN alpha to bind specifically to human cells. A BoIFN alpha molecule mutated in the 10-44 NH2-terminal domain was obtained which is 15, 8, and 35% as active as HuIFN-alpha J1 on human cells in specific binding, induction of antiviral, and 2-5A-synthetase activities, respectively. We concluded that at least 5 of the 12 residues at positions 10; 21, 22, 24; 27; 31, 34, 35, 37, 40; 42, 43 in the 10-44 NH2-terminal domain are critical for recognition of the human IFN-alpha cell receptor and for biological activity. These residues are found among 10 strictly conserved residues in all reported mammalian IFN alpha S, and they act in a cooperative manner to induce a biological response in human cells. The gap between the extent of improvement in binding capacity of the BoIFN alpha mutants on human cells and the corresponding biological response suggests that the primary signal of binding to the cell receptor is amplified within the cell. On bovine cells, HuIFN-alpha J1 and BoIFN-alpha C also compete for the same receptor, and it seems that at least part of the 10-44 NH2-terminal domain on IFN alpha is also involved in interaction with the bovine IFN alpha cell receptor.

2',5'-Oligoadenylate Synthetase↗
PubMed1987

Differential effects of interferon-alpha and interferon-gamma on interleukin 1 secretion by monocytes.

We examined the effect of interferon (IFN)-alpha and IFN-gamma on the ability of human monocytes to secrete interleukin 1 (IL 1). IFN-alpha directly induced IL 1 secretion by monocytes. IFN-gamma did not induce any IL 1. IFN-gamma-stimulated monocyte supernatants were also negative for pyrogenic activity. However, IFN-gamma greatly enhanced the amount of IL 1 secreted when monocytes were stimulated by lipopolysaccharide or Staphylococcus aureus, even at concentrations which by themselves did not induce IL 1. IFN-alpha did not enhance IL 1 secretion induced by other stimuli. IFN-gamma enhanced IL 1 secretion by priming monocytes to be more sensitive to an IL 1-inducing stimulus. However, IFN-gamma does not enhance IL 1 induced by all stimuli, because there was no enhancement of IL 1 induced by PMA. Thus, IFN-alpha and IFN-gamma have very distinct roles in the induction and enhancement of IL 1 by monocytes.

Humans↗
PubMed1979

Augmentation of mouse natural killer cell activity by interferon and interferon inducers.

Interferon (IF), in addition to its anti-viral capacity, is increasingly being found to be a regulator of cell division, cell surface antigens, and cell function. To determine whether IF also plays a role in the regulation of natural killer (NK) cell activity in mice, the in vivo and in vitro effects of IF and IF inducers on NK activity were studied. We observed that pyran, lipopolysaccharide, and polyinosinicopolycytidylic acid (poly I:C) as well as crude and purified IF preparations significantly elevated splenic NK levels in normal mice within 3 to 24 hr of i.p. administration. Normal spleen cells treated with poly I:C or IF in vitro also had augmented NK activity. Poly I:C and IF were themselves not cytotoxic and their presence was not required during the lytic process, indicating that IF acts on lymphocytes to activate NK function. The addition of anti-IF in the incubation medium completely blocked the boosting of NK activity by poly I:C or IF. The characteristics of the effector cells activated by IF were consistent with those of NK cells rather than macrophages, since the boosted effector cells were not retained by a rayon column or removed by carbonyl iron. Moreover, they were resistant to treatment with anti-Thy 1.2 serum plus complement, which eliminated mature T cells.

Animals↗
PubMed1987

Synergistic antiproliferative effect of recombinant alpha-interferons with recombinant gamma-interferon.

Two human tumor cell lines were studied for their response to the antiproliferative effect of recombinant human interferons (IFNs) alpha 2, alpha 4, a hybrid alpha (delta 4 alpha 2 Bgl II alpha 1), and gamma, individually and in combination. Natural human alpha-IFN was used as a reference point for all experiments. RT4 (bladder carcinoma) cells were overall more sensitive to the antiproliferative effects of the IFNs than A2182 (lung adenocarcinoma) cells. Three-way analysis of variance indicated that the relative effectiveness of the alpha-IFNs was alpha 2 less than alpha 4 less than hybrid alpha less than natural alpha-IFN. On an international reference unit per milliliter basis, gamma-IFN was 50- and 75-fold more effective than natural alpha-IFN and hybrid alpha-IFN in RT4 cells and 5.6-, 12.1-, and 14.9-fold more effective than alpha 4-, hybrid alpha-, and natural alpha-IFN in A2182 cells. In contrast, when recalculated on a nanogram per milliliter basis, gamma-IFN was only threefold more effective than the hybrid alpha-IFN in RT4 and approximately twofold less effective than alpha 4 and the hybrid alpha in A2182. Combinations of alpha-IFNs gave additive or antagonistic effects. When any of the alpha-IFNs were combined with the gamma-IFN, however, a synergistic antiproliferative effect was seen. The magnitude of the synergy was dependent upon the concentration of gamma-IFN used and the type of alpha-IFN in the combination. Antagonistic effects were seen at the lowest gamma-IFN concentration studied (0.2 IRU/ml). Synergy also varied according to the potency of the alpha-IFN used.

Carcinoma↗
PubMed1987

Interferon-gamma, interferon-alpha/beta, and tumor necrosis factor differentially affect major histocompatibility complex class I expression in murine leukemia virus-induced tumor cell lines.

Tumor cell lines induced by Gross murine leukemia virus were examined for cell-surface major histocompatibility complex class I expression. Three of five cell lines constitutively express H-2K and H-2D class I protein. Culturing these cells with interferon (IFN)-gamma, IFN-alpha/beta, or tumor necrosis factor increases both K and D expression in these cell lines. Two of five tumor cell lines express no class I proteins by fluorescence-activated cell sorter analysis, specific immunoprecipitation, and specific hybridization in Northern analysis. Treatment with IFN-gamma induces D, but not K protein expression in one of these cell lines. IFN-alpha/beta and tumor necrosis factor induce neither D nor K expression in this cell line. Thus, these two cytokines appear to have different mechanisms of action than IFN-gamma for altering class I expression. The other class I-negative tumor cell line does not express either K or D proteins under any conditions tested. All five cell lines express beta 2-microglobulin; this expression is increased by IFN-gamma treatment even in cell lines which do not express class I heavy chain. The results of this study demonstrate that 1) different tumor cell lines demonstrate variations in class I gene regulation, and 2) differences in regulation between class I genes may occur within a single cell line.

AKR murine leukemia virus↗