Selenium and vitamin E enriched diet increases NK cell cytotoxicity in cattle / Dieta enriquecida com selênio e vitamina E aumenta a citotoxicidade de células NK em bovinos

A number of studies has shown that antioxidants, fatty acids and trace minerals may modulate different immune cell activities, and that their deficiency may be associated with diseases and impaired immune responses. In innate immunity, natural killer (NK) cells have a central role, killing virally infected and cancerous cells, and also secreting cytokines that shape adaptive immune responses. Thus, the aim of this study was to evaluate the effect of enriched diets in selenium plus vitamin E and/or canola oil on complete blood count and on NK cell cytotoxicity from blood lymphocytes of Nellore bulls. Bulls that received selenium plus vitamin E had (P=0.0091) higher NK cell cytotoxicity than control bulls. This result positively correlated with serum selenium levels. To the best of our knowledge, this is the first study that showed immunostimulatory effects of selenium plus vitamin E on NK cell cytotoxicity of Nellore bulls.(AU)

Vários estudos demonstraram que antioxidantes, ácidos graxos e minerais podem modular a atividade de diferentes células do sistema imunológico e que as suas carências podem estar associadas a doenças e a respostas imunes comprometidas. Na imunidade inata, os linfócitos natural killer (NK) têm um papel central matando células infectadas por vírus e células cancerígenas, ao mesmo tempo em que também secretam citocinas que modulam as respostas imunes adaptativas. Assim, o objetivo deste estudo foi avaliar o efeito de dietas enriquecidas em selênio e vitamina E e/ou óleo de canola no hemograma e na citotoxicidade das células NK do sangue de bovinos da raça Nelore. Os animais que receberam selênio e vitamina E tiveram (P = 0,0091) maior citotoxicidade das células NK do que os animais do grupo controle. Este resultado foi positivamente correlacionado com os níveis de selênio no sangue. Para o melhor do nosso conhecimento, este é o primeiro estudo que mostrou efeitos imunoestimulatórios do selênio e vitamina E sobre a citotoxicidade das células NK de bovinos Nelore.(AU)

Lymphokine activated killer cells from peripheral blood mononuclear cells of endometriosis of patients improve cytotoxicity to endometriosis cell culture.

Background: To assess the increased cellular immunity of Peripheral Blood Mononuclear Cells (PBMC) derived LAK cells from endometriosis patients towards endometriosis cell cultures after stimulation with IL-2. Methods: This study is a quasi-experimental study of pre and post treatment using controls. Phenotype evaluation of CD3+CD4+, CD3+CD8+ and CD56+ effector cells of PBMC from endometriosis patients and controls was performed. Cytotoxicity test of PBMC from endometriosis patients and control towards Daudi, K562 cell line and endometriosis cell cultures using 51Chromium release assay was also carried out. Results: Phenotype evaluation of PBMC from endometriosis patients (n = 10) and controls (n = 6) were done prior to and after IL-2 stimulation. Before IL-2 stimulation, CD3+CD4+, CD56+ from endometriosis group (n = 10) tend to be lower than control (n=6) whereas CD3+CD8+ were higher in endometriosis group than controls. After IL-2 stimulation, CD3+ CD8+, CD56+ of PBMC from endometriosis group were significantly increased (p < 0.05). Cytotoxicity test revealed a significant increase (p < 0.05) in both PBMC’s effector cells from endometriosis and control group towards target cells, Daudi, and K562 cell lines after IL-2 stimulation. PBMC’s effector cells cytotoxicity from both endometriosis and control towards target endometriosis cell cultures were also elevated after IL-2 stimulation. Conclusion: LAK cells derived IL-2 stimulated PBMC from endometriosis patients increased cellular immunity towards endometriosis cell cultures.

Immunological effector cells enhance apoptosis induced by adriamycin in a multi-drug resistant human breast cancer cell line / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To investigate the effects of immunologic effector cells to enhance apoptosis induced by adriamycin (ADR) in multi-drug resistant human breast cancer cell line MCF7/ADR.</p><p><b>METHODS</b>The immunologic effector cells were induced and expanded by IFN-gamma, McAb CD3, IL-1 and IL-2. The expression of P-glycoprotein (P-gp) and its relation to apoptosis in target cells were detected by TUNEL technique and immunohistochemical staining. Flow cytometry (FCM) was carried out to determine the expression level of human breast cancer related P185 antigen and the positive rate of Annexin V-FITC/PI expression. The subcellular distribution of ADR and Annexin V expression in the target cells were detected by fluorescence microscopy.</p><p><b>RESULTS</b>The immunologic effector cells down-regulated the expression of P185 and P-gp in MCF7/ADR cells. The accumulation and subcellular distribution of ADR in MCF7/ADR cells were increased after co-culture with the immunologic effector cells. After treatment with the immunologic effector cells in combination with ADR, apoptosis rate of the target cells was 10 times higher than that induced by ADR alone, and 13 times higher than that induced by the immunologic effector cells alone.</p><p><b>CONCLUSION</b>Immunologic effector cells can simultaneously down-regulate the expression of P185 and P-gp in MCF7/ADR cell line, and increase the apoptosis rate of MCF7/ADR cells in combination with ADR.</p>

Killing activity in DC and CIK co-culture against hepatocarcinoma cells / 中国实验血液学杂志

This study was aimed to investigate the proliferation activities and phenotype changes of DC, CIK and DC-CIK, and their cytotoxicity against hepatocarcinoma cells in co-culture of DC with CIK. Peripheral blood mononuclear cells (PBMNC) were isolated from healthy adult donors. After incubation of PBMNC for 2 hours, DCs were induced from adherent cells by some cytokines and CIKs were generated from non-adherent cells. Mature DCs were harvested after incubation for 9 days, and then were co-cultured with CIK at ratio of 1:5 for 3 days. The cytotoxicity activity against SMMC-7721 hepatocellular carcinoma cell line was detected by MTT assay. The results showed that CIK cells were able to lyse SMMC-7721 hepatocellular carcinoma cells at low ratios of effector to target. This effect was significantly enhanced by co-culture with DCs. It is concluded that CIK cells have high lytic activity against 7721 hepatocellular carcinoma cell line, which can be enhanced by co-culture with DC. DC-CIK cells are highly effective immune cells.

La vía de CD1 y la activación de células T NK hacia los antígenos glicolipídicos de Mycobacterium tuberculosis / CD1 pathway and NK T Cell activation to glycolipid antigens from Mycobacterium

El objetivo de esta revisión es analizar el estado actual de nuestro conocimiento sobre las moléculas de superficie celular involucradas en la presentación de antígenos glicolipídicos, denominadas familia CD1. Estas proteínas constituyen la tercera clase de moléculas presentadoras de antígeno. Las proteínas CD 1 controlan diversas funciones inmunes importantes en la defensa del hospedero contra las infecciones microbianas. En años recientes estas proteínas han sido involucradas en la generación de una respuesta inmune celular contra Mycobacterium tuberculosis. Aquí, nosotros analizaremos aspectos relevantes acerca de las proteínas CD 1 y las células T específicas para antígenos glicolipídicos.

The aim of this review is to analyze the current state of our knowledge about cell surface molecules involved in glycolipid antigen presentation, named CD1 family. These proteins constitute a third class of antigen-presenting molecules. CD 1 molecules develop diverse important immune functions in host defenses against microbial infections. In recent years these proteins have been involved in the generation of cell-mediated immune response against Mycobacterium tuberculosis. Here, we analyze relevant roles of CD1 proteins and glycolipid antigen-specific T cells.

E. coli-based production of recombinant HMG-17 and its antibacterial domain / 生物医学工程学杂志

Total RNA was extracted from human LAK cell, and a cDNA encoding mature peptide HMG-17 and its alpha helix domain was amplified by RT-PCR. The recombinant prokaryotic expression vector pGEX-1lambdaT-HMG-17 and pGEX-1lambdaT HMG-17alpha helix was constructed. Using affinity chromatography, thrombin cleaving and AU-PAGE elution, we obtained the purified HMG-17. Analyses of MIC, MEC and MBC indicated that HMG-17 and HMG-17alpha had strong antibacterial activity. MIC of the alpha-helic domain was almost the same as that of HMG17, suggesting that the alpha-helic structure would be essential for the antibacterial activity of HMG-17.

The effect of tumor-dendritic cell fusion vaccines on the cytotoxicity of CIK/NK cells from cord blood / 中华血液学杂志

<p><b>OBJECTIVES</b>To evaluate the effects of K562-dendritic cell (DC) and Raji-DC fusion vaccines on the cytotoxicity of cord blood (CB) derived cytokine-induced killer/natural killer (CIK/NK) cells.</p><p><b>METHODS</b>DC and CIK/NK cells were derived from CB mononuclear cells. CB-DC were fused with inactivated K562 or Raji cells by PEG to form K562 or Raji-DC fusion vaccine. The CIK/NK cells stimulated by different co-culture antigens were three groups: K562-DC or Raji-DC fusion vaccine group, inactivated K562 or Raji plus DC group, and CB-DC alone group. The cytotoxicity of CIK/NK cells stimulated by different co-culture antigens was measured by MTT test.</p><p><b>RESULTS</b>All the antigens used for stimulation could enhance the cytotoxicity of CB-CIK/NK cells, with no specificity difference. At 20:1 effector-target ratio, the cytolytic activities of K562-DC and Raji-DC fusion vaccine groups against Raji cells were (75.44 +/- 4.19)% and (81.33 +/- 4.18)% respectively (P < 0.05); and that of inactivated K562 + DC and Raji + DC group against Raji cells were (73.12 +/- 4.22)% and (80.49 +/- 4.27)%, respectively (P < 0.01). There was no significant difference in the cytotoxicity to K562 cells between the two fusion vaccine groups (P > 0.05). The cytotoxicity of CB-CIK/NK cells immunized by Raji cells was higher than that by K562 cells. In CIK/NK cells co-stimulated by the same tumor antigen, there was no significant difference in the cytotoxicity between DC fusion vaccine group and inactivated cells plus DC group to different tumor cells.</p><p><b>CONCLUSIONS</b>The cytotoxicity of CB-CIK/NK cells to tumor cells was not specific. There was no significant difference in the cytotoxic activity of CB-CIK/NK cells between the DC fusion vaccine group and inactivated cells plus DC group.</p>

Effect of phytohemagglutinin on proliferation and cytotoxicity of cytokine-induced killer cells / 中国实验血液学杂志

The purpose was to investigate the effect of phytohemagglutinin (PHA) on proliferation and cytotoxicity of cytokine-induced killer (CIK). Peripheral blood mononuclear cells (PBMNCs) from healthy donors were divided into two groups. Cells were resuspended and maintained in complete medium containing of 10% autologous plasma. CIK cells were cultured by traditional method in group one. The other group cells were added PHA to stimulate PBMNCs for 24 hours, then cultured like incubating CIK cells. Their cytotoxicity to different target cells was evaluated by (51)Cr release assay. The results showed that the proliferation multiples of CIK and PHA-CIK cells were both high, however, the latter was much higher than CIK with significance (P < 0.05). Cells in each group cells showed high cytotoxicity. At the same high effector/target ratio PHA-CIK cells cytotoxicity was stronger than CIK cells when targets were K562 cells or acute leukemia cells (P < 0.05). In conclusion, PHA-CIK cells exhibit stronger proliferation and cytotoxicity than CIK cells, and the result provides an experimental basis for biotherapy.

Effect of tamoxifen on estrogen receptor negative breast cancer cells

This study was undertaken to investigate the mechanism[s] underlying the use of tamoxifen [TAM], a selective estrogen receptor modulator [SERM], in estrogen receptor [ER] negative breast cancer and to assess the role of TAM on lymphokine activated killer [LAK] cells reactive to autologous breast cancer cells. Twenty female breast cancer patients attending the outpatient clinic of the Medical Research Institute were enrolled in this study. All patients had modified radical mastectomy. Pieces of fresh breast tumor cells and their in vitro generated autologous LAK were treated with different doses of TAM prior to or during the cytotoxicity assay. Estrogen receptors were measured using the enzyme immunoassay kit. Treatment of effector cells with TAM did not affect their lytic function against their autologous breast cancer cells, irrespective of their ER state. However, TAM pretreatment of ER positive breast cancer cells resulted in their significant lysis by their autologous LAK cells. The degree of enhancement was directly proportional to the dose of TAM. On the other hand, pretreatment of ER negative breast cancer cells with TAM did not affect their lytic response to autologous LAK cells. An enhanced cytolytic effect was only observed for ER negative breast cancer cells when TAM was directly added to the cytotoxicity assay, indicating an indirect mode of action through the release of mediators. The data provide an evidence of a dual mechanism of action of TAM, one direct, which is evident against ER positive cancer cells while the other is indirect through the release of mediators. This might explain the usefulness of selective estrogen receptor modulators in ER negative breast cancer patients

Generation of T cell-mediated antitumor response in vitro by autologous dendritic cells pulsed with tumor lysates in patients with non-small cell lung cancer / 中华肿瘤杂志

<p><b>OBJECTIVE</b>To investigate whether dendritic cells pulsed with whole tumor lysates (WTL) could in vitro elicit antitumor T cell responses in patients with non-small-cell lung cancer (NSCLC).</p><p><b>METHODS</b>Monocyte-derived immature DCs (imDCs) generated in the presence of human recombinant granulocyte-macrophage colony stimulating factor and interleukin-4 from peripheral blood mononuclear cell of NSCLC patients, and then were induced to mature by pulsing autologous WTL (DCs/WTL) or by the addition of TNF-alpha(TNF/DCs). FACS and MLR assay were used to monitor their phenotypic changes and capacity to stimulate allogeneic and autologous T cell proliferation. DCs/WTL activated with TNF-alpha (* DCs/WTL) were cocultured in vitro with autologous T cells for eliciting antitumor CTLs. T cell mediated antitumor responses were measured by IFN-gamma enzyme-linked immunospot (ELISPOT) assay for WTL-specific IFN-gamma releasing T cells and by lactate dehydrogenase release (LDH) assay for lysis of autologous tumor cells, respectively.</p><p><b>RESULTS</b>When monocytes-derived imDCs from the patients with NSCLC (n = 10) were pulsed with autologous WTL for a day at 30 microg total protein of WTL per 10(6) DCs/ml, this led to up-regulation of CD1a, CD83 and CD86 as well as HLA-DR, and also led to marked stimulation of allogeneic T cell proliferating activity, which was comparable to that of TNF/DCs. However, their capacity of stimulating autologous T cell proliferation in vitro was significantly more potent than those of TNF/DCs (P < 0.05). The numbers of WTL-specific IFN-gamma releasing T cells in 1/3 cultures after one week exposure to * DCs/WTL was increased significantly compared with those pulsing with TNF/DCs plus IL-2 or IL-2 alone (P = 0.05). T cells derived by priming of non-adherent PBMCs with * DCs/WTL after 14 days in vitro stimulation were significantly more responsive to autologous tumor cells compared with LAK (n = 3, P < 0.05), but its cytotoxicity against K562 cells was also comparable to LAK cells.</p><p><b>CONCLUSION</b>Monocyte-derived DCs from NSCLC patients could serve as functional APC. The * DCs/WTL may effectively elicit T cell-mediated antitumor response in vitro and enhance NK killing activity.</p>

Specific anti-leukemic cell effect mediated by dendritic cells pulsed with chronic myelogenous leukemia lysate antigen in vitro / 中国实验血液学杂志

To investigate the specific antileukemia effect of dendritic cells (DC) pulsed with chronic myelogenous leukemic lysate antigen (CLA), dendritic cells from patients with chronic myelogenous leukemia (CML) were pulsed by CLA, and then cocultured with cytokine-induced killer (CIK) cells from CML patients (CIK + CLA-DC group). The cytotoxic activity in vitro was measured by using a lactate dehydrogenase release assay, and compared with CIK + DC, CIK and CIK + CLA groups. The results showed that under an effector-target ratio of 25:1, the cytotoxic activity of CIK + CLA-DC, CIK + DC, CIK and CIK + CLA groups against autologous CML cells was (68.8 +/- 14.2)%, (52.5 +/- 9.4)%, (20.6 +/- 7.5)% and (24.2 +/- 8.7)%, respectively. CIK + CLA-DC group displayed a strongest cytotoxic activity. When K562 and Raji cells acted as target cells and CIK as effectors, the cytotoxic activity against autologous CML cells in CIK + CLA-DC group (68.8 +/- 14.2)% was much higher than that against K562 cells (14.6 +/- 6.2)% and Raji cells (12.7 +/- 10.2)%, respectively. In conclusion, coculture of CIK cells with DC led to a significant increase in cytotoxic activity. The cytotoxicity could be further increased by DC pulse with CML cell lysate antigen, and cytotoxicity mediated by CML lysate antigen possess stronger specificity.

Cytokine-induced killer cells induce apoptosis of K562 cells expressed bcr-abl / 中国实验血液学杂志

In order to investigate whether cytokine-induced killer (CIK) cells can induce apoptosis of bcr-abl(+) K562 cells, apoptosis of K562 cells and CEM cells induced by CIK cells, etoposide or camptothecin was detected with flow cytometry DNA assay. RT-PCR showed that K562 cells expressed the bcr-abl fusion gene, K 562 cells, K562 cells/etoposide or K562 cells/camptothecin groups showed no sub-G(1) peak. K562 cells/CIK cells group showed sub-G(1) peak (38.1%). CEM cells showed no sub-G(1) peak. CEM cells/camptothecin or CEM cells/etoposide groups showed sub-G(1) peak (23.5% or 32.3% respectively). CEM cells/CIK cells group showed sub-G(1) peak (45.4%). Etoposide or camptothecin did not induce apoptosis of K562 cells. CIK cells induce apoptosis of K562 cells. Bcr-abl fusion gene prevented apoptosis induced by etoposide or camptothecin, but did not prevent apoptosis induced by CIK cells. This property may support the observed adoptive immunologic effect of allogeneic bone marrow transplantation and donor lymphocyte transfusions of CML case relapsing after allogeneic bone marrow transplantation.

Immunoprotective effect of IL-2 and B7-1 gene co-transfected liver cancer vaccines on hepatocarcinogenesis in mice / 中华肝脏病杂志

<p><b>OBJECTIVE</b>To study the immunoprotective effect of IL-2 and B7-1 gene co-transfected liver cancer vaccine on hepatocarcinogenesis in mice.</p><p><b>METHODS</b>The murine liver cancer cell strain Hepal-6 was transfected with IL-2 and/or B7-1 gene via recombinant adenovirus vectors and the liver cancer vaccines were prepared. C57BL/6 mice were immunized with the vaccines and challenged with the parental Hepal-6 cells afterwards. The immunoprotection was investigated and the reactive T cell line was assayed.</p><p><b>RESULTS</b>The effect of the Hep6-IL2/B7 vaccine on the onset of tumor formation was the strongest. The media survival time of the mice was the longest (68 days, P<0.05) and the implanted tumor was the smallest (P<0.05). The effect of single IL-2 or B7-1 gene-transfected vaccine was next to the co-transfected gene group with the mean survival time being 59 and 54 days, respectively. The mean survival time of wild or BGFP gene modified vaccine immunized group was 51 and 48 days, respectively. The control group all died within 38 days and the implanted tumor was the largest (P<0.05). The cellular immunofunction test and cytotoxicity study showed that the mice immunized with the Hep6-IL2/B7 vaccine gained significantly increased NK, LAK and CTL activity (29.0% +/- 2.5%, 65.0% +/- 2.9%, 83.1% +/- 1.5% respectively, compared with other groups P<0.05).</p><p><b>CONCLUSIONS</b>The IL-2 and B7-1 gene co-transfected liver cancer vaccines can induce the mice to produce activated and specific CTL against the parental tumor cells, and demonstrate stronger effect on the hepatocarcinogenesis than single gene modified or the regular tumor vaccine. Therefore, the vaccines may become a novel potential therapy for recurrence and metastases of HCC.</p>

Effect of target cell nitric oxide synthesis on the sensitivity to lymphokine-activated killer cell cytotoxicity

BACKGROUND: Nitric oxide (NO), a cytotoxic molecule is produced in various tissues including tumor cells during interleukin-2 (IL-2) therapy . Lymphokine-activated killer (LAK) cells are induced during IL-2 therapy, and have cytotoxic activity against tumor cells. The current study investigated the effects of NO synthesized in target cells or exposure of target cells to NO on the sensitivity of target cells to LAK cell cytotoxicity. METHODS: Cytotoxicity was measured using 4 h chromium release assays. LAK cells which were induced by a 4 day incubation of BALB/c mouse splenocytes with IL-2 (6,000 IU/mL) were employed as effector cells. RD-995 skin tumor cells originated from a C3H/HeN mouse were employed as target cells. NO synthesis in target cells was induced by a 24 h incubation of RD-995 cells with IFN gamma (25 U/mL), TNF (50 U/mL) and IL-1 (20 U/mL). S-nitrosyl acetylpenicillamine (SNAP), an NO donor, was used to expose target cells to NO. N(G) -monomethyl-L-arginine (MLA) and carboxy-PTIO were added during cytotoxicity assays to inhibit NO synthesis, and to scavenge NO produced by target cells, respectively. RESULTS: Sensitivity of NO-producing RD-995 cells to LAK cell cytotoxicity was decreased by addition of MLA and carboxy-PTIO during cytotoxicity assays. However, the two reagents had no effect on the sensitivity of non-NO-producing RD-995 cells. Pretreatment of RD-995 target cells with SNAP increased the sensitivity in comparison with untreated cells. CONCLUSIONS: Sensitivity of target cells to LAK cell cytotoxicity is increased by target cell NO synthesis or exposure to NO. Further studies are needed to evaluate whether these in vitro results have relevance to in vivo phenomena.

Anti-fungal and cytokine producing activities of CD8 + T lymphocytes from HIV-1 infected individuals

Lymphokine activated killer (LAK) cells are capable of killing not only malignant cells but also hyphal form of Candida albicans in vitro. When peripheral blood mononuclear cells (PBMC) from normal healthy donors were cultured for 72-96 hrs with 1,500 international unit (IU)/ml interleukin-2 (IL-2), marked LAK activity was induced. However, even prior to IL-2 activation, PBMC isolated from some normal subjects and those from almost all individuals who are infected by human immunodeficiency virus type 1 (HIV-1) exhibited significant levels of anti-fungal activity. Such pre-activation in situ antifungal activity of PBMC decreased during the initial 48 hrs of IL-2 activation. PBMC from HIV-1 seropositive subjects showed higher levels of in situ anti-fungal activity than normal PBMC did. After a decline of in situ activity during the initial 48 hours, LAK activity gradually increased and reached near maximal levels by day 4 and remained more or less constant until day 6. No significant difference was observed between the LAK activity of normal and HIV-1(+) PBMCs on days 4-6. In IL-2 activated normal and HIV-1(+) PBMC cultures, both CD4 and CD8 T cells produced IL-2, INF-gamma as well as TNF-alpha. Production of IL-2 by both CD4 and CD8 T cells was suppressed in HIV-1(+) PBMC cultures, but no significant suppression of INF-gamma production was noted. Meanwhile, TNF-alpha production by CD4 was very much suppressed but no significant changes in TNF-alpha production by CD8 T cells was noted in HIV-1(+) PBMC cultures

The effect of interleukin 2 on the induction Of Nk 1.1 expression in CD8+ and CD4-CD8-T Cell / 천식및알레르기

BACKGROUND: Murine IL-2-induced lymphokine-activated killers can be divided into two mutually exclusive subset:NK1.1'CD8 and NK1.1 CD8+. However, there is a strong evidence that NK cell may belong to T cell lineage. Recently novel lymphocyte subsets, present in the adult murine thymus, CD3+NK1.1'TCRap(TNK) cell is readily identifiable in fresh obtained murine adult CD4 CD8 thymocytes. MATERIAL AND METHOD: We sorted out CD4 and CD8 (double negative.' DN) cells and CD8+ cells from murine spleen and cultivated these cells with IL-2. And the surface B220, CD8, NK1. 1 and cytopasmic NK1.1 was analysed simultaneously to see whether these cells can be switched to the other subtype of cells. RESULT: Purified DN cells were switched to several subtype of cells'. CD8'B220+(LAK cells), NK1.1'B220+(LAK cells), CD8 B220, cytoplasmic NK1.1+B220 cells. Purified CD8 cells were switched to CD8+B220' LAK cells and cytoplasmic NK1.1+ CD8+ B220+ and cytoplasmic NK1.1' CD8 B220 cells. In addition, the CD8' cells originated from DN cells do not express the cytoplasmic NK1.1 in contrary to the sorted CD8 cells. CONCLUSION: Our results indicated that these will be useful models to investigating CD8 precursor potentials in populations of CD4 CD8 (doble negative) cells and relationship of NK1.1 These results also supports the hypothesis that T cells and NK cells have same ontogeny and CD8 effector functions are potentially diverse and could be exploited by various conditions that switch off host protected cytolytic response. These model offer a way to study the molecular regulation of CD8 gene expression.

Effect of gamma interferon on the expression of class I MHC antigens on fresh leukemic cells and their susceptibility to lysis by lymphokine activated killer cells.

Relationship between MHC class I antigen expression on PBLs from leukemia patients and their susceptibility to lysis by LAK cells was investigated. LAK cells induced small yet significant lysis of leukemic cells. In nine out of 14 cases studied, treatment with Interferon gamma (200 U/ml for 48 hours) resulted in a decrease in the LAK susceptibility of leukemic cells. In six of these cases, there was a concomitant increase in the expression of class I MHC antigen expression. In three samples, the increase in MHC class I antigen expression was not accompanied by a decrease in LAK susceptibility. IFN treatment had no effect on the binding of leukemic cells to LAK effector cells.