Insights into the Roles of Natural Killer Cells in Osteoarthritis.

Osteoarthritis (OA) is now widely acknowledged as a low-grade inflammatory condition, in which the intrinsic immune system plays a significant role in its pathogenesis. While the involvement of macrophages and T cells in the development of OA has been extensively reviewed, recent research has provided mounting evidence supporting the crucial contribution of NK cells in both the initiation and advancement of OA. Accumulated evidence has emerged in recent years indicating that NK cells play a critical role in OA development and progression. This review will outline the ongoing understanding of the utility of NK cells in the etiology of OA, focusing on how NK cells interact with chondrocytes, synoviocytes, osteoclasts, and other immune cells to influence the course of OA disease.

Functional molecular expression of nature killer cells correlated to HBsAg clearance in HBeAg-positive chronic hepatitis B patients during PEG-IFN α-2a therapy.

Objective: To explore whether the frequencies and functional molecules expression of Natural Killer cells (NK cells) are related to hepatitis B surface antigen (HBsAg) disappearance in hepatitis B e envelope antigen (HBeAg)-positive patients with chronic hepatitis B (CHB) throughout peginterferon alpha-2a (PEG-IFN α-2a) treatment. Methods: In this prospective research, HBeAg-positive patients with CHB received PEG-IFN α-2a treatment, completing 4-year follow-up. After PEG-IFN α-2a treatment, undetectable HBV DNA, HBsAg loss, and HBeAg disappearance were defined as functional cure. Proportions of NK, CD56dim, CD56bright, NKp46+, NKp46dim, NKp46high, and interferon alpha receptor 2 (IFNAR2)+ NK cells, and the mean fluorescence intensity (MFI) of NK cell surface receptors IFNAR2 and NKp46 were detected. Results: 66 patients were enrolled into the study in which 17 patients obtained functional cure. At baseline, hepatitis B virus desoxyribose nucleic acid (HBV DNA) titer in patients with functional cure was remarkably lower than that in Non-functional cure group. Compared with baseline, HBV DNA levels, HBsAg levels, and HBeAg levels significantly declined at week 12 and 24 of therapy in patients with functional cure. At baseline, the negative correlation between CD56bright NK% and HBV DNA and the negative correlation between CD56dim NK% and HBV DNA was showed; CD56bright NK% and IFNAR2 MFI in patients with functional cure were remarkably higher than those in patients without functional cure. After therapy, CD56bright NK% and NKp46high NK% in patients with functional cure were higher than those in patients without functional cure. In Functional cure group, after 24 weeks of treatment NK%, CD56bright NK%, IFNAR2 MFI weakly increased, and NKp46high NK% and NKp46 MFI significantly increased, meanwhile, CD56dim NK% and NKp46dim NK% decreased. Only NKp46 MFI increased after therapy in patients without functional cure. Conclusion: The lower HBV DNA load and the higher CD56bright NK% before therapy, and the higher the post-treatment CD56bright NK%, IFNAR2 MFI, NKp46high NK%, the easier to achieve functional cure.

Human poliovirus receptor contributes to biliary atresia pathogenesis by exacerbating natural-killer-cell-mediated bile duct injury.

BACKGROUND AND AIMS: Natural killer (NK) cells play an important role in biliary atresia (BA) pathogenesis; human poliovirus receptor (PVR) is an important NK-cell modulator. Here, we explored the role of PVR in BA pathogenesis. METHODS: Poliovirus receptor expression and NK cell-associated genes were detected in human BA samples and a rotavirus-induced BA mouse model using quantitative PCR and immunofluorescence staining. Chemically modified small interfering RNA silenced PVR expression in the BA model, and its effects on the population and function of intrahepatic NK cells were investigated using flow cytometry (FCM). The effects of PVR overexpression and knockdown on proliferation, apoptosis and NK-cell-mediated lysis of cultured human cholangiocytes were analysed using FCM and cell viability assays. Serum PVR, high-mobility group box 1 (HMGB1), and interleukin-1beta (IL-1beta) levels were measured in a cohort of 50 patients using ELISA. RESULTS: Poliovirus receptor expression was upregulated in the biliary epithelium of BA patients and BA model and was positively correlated with the population and activation of intrahepatic NK cells. Silencing of PVR expression impaired the cytotoxicity of NK cells, reduced inflammation and protected mice from rotavirus-induced BA. Activation of the TLR3-IRF3 signalling pathway induced PVR expression in cultured cholangiocytes. PVR overexpression promoted proliferation and inhibited the apoptosis of cholangiocytes but exacerbated NK cell-mediated cholangiocyte lysis. Serum PVR levels were elevated in BA patients and were positively correlated with HMGB1 and IL-1beta levels. CONCLUSIONS: Poliovirus receptor contributes to BA pathogenesis by regulating NK cell-mediated bile duct injury; PVR has the value as a biomarker of BA.

Decreased CD57 expression of natural killer cells enhanced cytotoxicity in patients with primary sclerosing cholangitis.

Background/aims: Primary sclerosing cholangitis (PSC) is a chronic inflammatory biliary disease for which the immunopathological basis remains an enigma. Natural killer (NK) cells are key components of innate immunity and seemingly play diversified roles in different autoimmune disorders (AIDs). The aim of this study was to determine the role of NK cells in the pathogenesis of PSC. Methods: The frequency and phenotype of circulating NK cells in a large cohort of patients with PSC and healthy controls (HCs) were systematically examined. In addition, the functional capacity of NK cells including cytotoxicity and cytokine production was studied. Results: The frequency of CD3-CD56dimCD16+ (defined as CD56dim) NK cells in PSC patients was significantly lower in comparison to HCs. CD56dim NK cells from PSC displayed a more immature phenotype including high expression of the natural killing receptor NKp46 and downregulation of the highly differentiated NK cell marker CD57. Interestingly, the reduction of CD57 expression of NK cells was associated with the disease severity of PSC. In addition, PSC CD56dim NK cells exhibited increased CD107a degranulation and cytolytic activity toward target cells compared with HCs. Further analysis demonstrated that CD57-CD56dim NK cells from PSC had elevated expression of NKp46, NKp30, IL-2 receptor, and KLRG1 and higher cytotoxic capacity as compared to CD57+CD56dim NK cells. Conclusions: Our data demonstrate that the differentiation of PSC NK cells is dysregulated with enhanced cytotoxic activity. This change is likely to be functionally involved in pathogenesis and disease progression, deducing the potential of NK-directed immunotherapy for PSC.

The effects of stereotactic body radiotherapy on peripheral natural killer and CD3+CD56+ NKT-like cells in patients with hepatocellular carcinoma.

BACKGROUND: Both natural killer (NK) and CD3+CD56+natural killer T (NKT)-like cells play critical roles in the antitumor response. This study aimed to explore the effects of stereotactic body radiotherapy (SBRT) on peripheral NK and NKT-like cells in patients with hepatocellular carcinoma (HCC), and to identify possible surface markers on these cells that correlate with the prognosis. METHODS: Twenty-five HCC patients were prospectively enrolled in our study, and 10 healthy individuals were served as healthy controls. Flow cytometry was used to determine the counts and the percentages of peripheral NK and NKT-like cells, cells with certain receptors, and cells with intracellular interferon-γ and TNF-α secretion at different time points, including time points of prior to SBRT, at post-SBRT, and 3-month and 6-month after treatment. The Kaplan-Meier method with the log-rank test was applied for survival analysis. RESULTS: The peripheral NKT-like cells was increased at post-SBRT. Meanwhile, elevated levels of inhibitory receptors and reduced levels of activating receptors of NK cells were also observed in NK cells at post-SBRT, but the levels was not significantly different at 3-month and 6-month as compared with the baseline levels. Lower percentage of NKp30+NK cells before SBRT and higher percentage of CD158b+NK cells after SBRT were associated with poor progression-free survival. In addition, higher percentage of CD3+CD56+ NKT-like cells was associated with a higher overall survival rate in HCC patients. CONCLUSIONS: SBRT has an apparent effect on both peripheral NK and CD3+CD56+NKT-like cells. Lower percentage of NKp30+NK cells before SBRT and higher percentage of CD158b+NK cells after SBRT are correlated with poor patients' PFS. Higher percentage of CD3+CD56+ NKT-like cells is associated with higher OS in HCC patients.

Circulating CD16+CD56+ nature killer cells indicate the prognosis of colorectal cancer after initial chemotherapy.

As the prognosis of colorectal cancer (CRC) does not always coincide with the pathology and/or surgical findings, a reliable noninvasive prediction tool for the prognosis of CRC is needed. Patients admitted for initial treatment of CRC between January 1, 2015 and December 31, 2015 were retrieved and reviewed. Records of circulating CD16+ CD56+ natural killer (NK) cells were analyzed before and after the initial chemotherapy of FOLFOX plan. Patients were followed up until June 30, 2019. One hundred and twenty-four cases after the FOLFOX chemotherapy were enrolled into this study. There were no significant differences in gender, age, or number of metastasis cases between the survival group and the nonsurvival group (p > 0.05), but significant differences in pre-chemotherapy, post-chemotherapy, and the differences between pre- and post-chemotherapy circulating CD16+ CD56+ NK cells between the survival group and the nonsurvival group (p < 0.01, p < 0.01, and p < 0.05, respectively) were observed. For the prediction of survival and nonsurvival CRC cases, the Areas Under the Curve were 0.626 and 0.759 in the Receiver-Operating Characteristic curves for the pre- and post-chemotherapy circulating CD16+ CD56+NK cells, respectively. Using an optimal cutoff value of 11.8% in post-chemotherapy circulating CD16+CD56+NK cells to differentiate survival and nonsurvival cases, the odds ratio was 0.12 (0.05, 0.27), p < 0.001. The percentages of both pre-chemotherapy and post-chemotherapy circulating CD16+CD56+NK cells were negatively correlated with the prognosis of CRC. The percentage of post-chemotherapy circulating CD16+CD56+NK cells was able to effectively predict the prognosis of CRC cases.

Selenium-containing ruthenium complex synergizes with natural killer cells to enhance immunotherapy against prostate cancer via activating TRAIL/FasL signaling.

Natural killer (NK) cells-based therapy has been used widely for cancer treatment in clinic trails. However, the immunotherapeutic efficacy of this method has been greatly hindered by tumor evasion and diminished activities of NK cells. In the present study, a selenium (Se)-bearing ruthenium (Ru) complex (RuSe) was designed that could synergistically potentiate NK cell-mediated killing against prostate cancer cells. As expected, pretreatment of cancer cells with subtoxic doses of RuSe effectively augmented the lysis potency of NK cells, with up to 2.46-fold enhancement than NK cells alone, against PC3 cells. More importantly, low concentrations of RuSe could augment the tumor destroying potency of NK cells derived from 10 clinical patients, with the enhancement range from 0.78- to 11.9-fold against PC3 cells and 0.67- to 3.8-fold against LNCAP cells. Mechanistic studies revealed that the sensitizing effect of RuSe primarily depended on TRAIL/TRAIL-R and Fas/FasL-mediated signaling. Furthermore, the increased expression level of these ligands highly relied on ROS overproduction-triggered DNA damage and the downstream ATM and ATR pathways. Furthermore, RuSe potently activated and synergized with NK cells to restrain tumor growth in vivo without causing toxic side effects on major organs. Taken together, the current study not only provides a strategy for application of metal complexes in chemo-immunotherapy but also sheds light on the potential roles and mechanisms of action on such Se-containing drugs as efficient immune-sensitizing agents for NK cell-based immunotherapy.

Hypoxia-inducible gene 2 promotes the immune escape of hepatocellular carcinoma from nature killer cells through the interleukin-10-STAT3 signaling pathway.

BACKGROUND: The study examines the expression and function of hypoxia-inducible gene 2 (HIG2) in hepatocellular carcinoma (HCC) tissues and cells. METHODS: Forty patients with HCC were included in the study. Bioinformatic analysis was used to analyze the clinical relevance of HIG2 expression in HCC tissue samples. Immunohistochemistry was employed to determine the expression of target proteins in tumor tissues. Hepatic HepG2 and SMMC-7721 cells were transfected with HIG2-targeting siRNA with Lipofectamine 2000. qRT-PCR was carried out to determine gene expression levels, while Western blotting was used to determine protein expression. A CCK-8 assay was performed to detect proliferation of cells, while migration and invasion of cells were studied by Transwell assay. Flow cytometry was carried out to detect surface markers and effector molecules in Nature killercells, as well as the killing effect of NK cells. RESULTS: HIG2 expression was upregulated in HCC. Silencing of HIG2 suppressed HCC cell migration and invasion. The killing effect of NK cells on HCC cells was enhanced after HIG2 was silenced in HCC cells. Conditioned media from HIG2-silenced SMMC-7721 cells inhibited the phenotype and function of NK cells. HCC cells with silenced expression of HIG2 modulated the activity of NK cells via STAT3. HIG2 promoted the evasion of HCC cells from killing by NK cells through upregulation of IL-10 expression. CONCLUSION: The study demonstrates that HIG2 activates the STAT3 signaling pathway in NK cells by promoting IL-10 release by HCC cells, thereby inhibiting the killing activity of NK cells, and subsequently promoting the recurrence and metastasis of HCC.

[Reduced frequency of natural killer cell on siglec-7(+) is associated with progression of hepatitis B virus-related cirrhosis].

Objective: To explore the relationship between sialic-acid-binding immunoglobulin-like lectin 7 (Siglec-7) expressed on NK cells and hepatitis B virus-related cirrhosis. Methods: Peripheral venous blood samples were collected from 23 healthy controls and 31 patients with hepatitis B virus-related cirrhosis (Child-Pugh A, n = 7; Child-Pugh B, n = 12; Child-Pugh C, n = 12). Peripheral blood mononuclear cells (PBMCs) were obtained by using Ficoll-Hypaque density gradient centrifugation and the expression of Siglec-7 and NK cells phenotype and their subpopulations were detected by flow cytometry. Comparisons between various groups were performed using t -test, one-way analysis of variance (ANOVA), and correlations between variables were analyzed using Pearson's-correlation coefficient. Results: (1) There was no significant difference in the percentage of NK cells and in their subpopulations with HBV-related cirrhosis and healthy controls. (2) Siglec-7 expression on NK cells in patients with HBV-related cirrhosis(62.44±13.45%)was significantly down-regulated than that to healthy controls(75.39±12.19%)while the frequency of Siglec-7(+) NK cells were negatively correlated with Child-Pugh score. (3) Subpopulation analysis showed that Siglec-7 expression on CD56(bright)CD16(-)NK cells(66.99±15.93%)was significantly lower than CD56(dim)CD16(+)NK cells(76.54±13.9%) in HBV-related cirrhosis. However, the expression of Siglec-7 in healthy controls showed no difference in these two NK cell subsets. (4) Phenotypic analysis showed that Siglec-7(+) NK cells express higher levels of activating receptor CD16, CD38, NKp46 and lower levels of inhibitory receptor CD158b. Indeed, the frequency of CD16 and CD38 on Siglec-7(+) NK cells in HBV-related cirrhosis was lower than that in healthy controls. Conclusion: The disease progression in patients with hepatitis B virus-related cirrhosis is associated to decreased frequencies of Siglec-7(+)NK cells.

Monomethylarsonous acid: Induction of DNA damage and oxidative stress in mouse natural killer cells at environmentally-relevant concentrations.

The carcinogenicity of arsenic has been confirmed in many studies, but its mechanism of action is still unclear. A lymphocyte component of the innate immune system, natural killer (NK) cells are responsible for killing cancer cells. Although inorganic arsenical species are the prevalent forms of arsenic in the environment, monomethylarsonous acid (MMA+3) is the major arsenical species found in immune-system cells, in this 30 d drinking-water-exposure study in mice. Therefore, the effect of MMA+3 on NK cells should be studied as a possible contributor to arsenic-induced toxicity at environmental exposure levels. In the mouse drinking-water-exposure model, As+3 induces dose-dependent DNA damage in NK cells. In in vitro studies, MMA+3 inhibited cell growth and induced DNA damage and oxidative stress at low concentration (20 and 50 nM) in isolated mouse NK cells. Strong correlations were found between DNA damage and oxidative stress in MMA+3-treated mouse NK cells. Even at low concentrations relevant to environmental arsenic exposures, MMA+3 is genotoxic to primary mouse NK cells.

Reduced frequency of natural killer cell on siglec-7+ is associated with progression of hepatitis B virus-related cirrhosis / 中华肝脏病杂志

Objective@#To explore the relationship between sialic-acid-binding immunoglobulin-like lectin 7 (Siglec-7) expressed on NK cells and hepatitis B virus-related cirrhosis.@*Methods@#Peripheral venous blood samples were collected from 23 healthy controls and 31 patients with hepatitis B virus-related cirrhosis (Child-Pugh A, n = 7; Child-Pugh B, n = 12; Child-Pugh C, n = 12). Peripheral blood mononuclear cells (PBMCs) were obtained by using Ficoll-Hypaque density gradient centrifugation and the expression of Siglec-7 and NK cells phenotype and their subpopulations were detected by flow cytometry. Comparisons between various groups were performed using t -test, one-way analysis of variance (ANOVA), and correlations between variables were analyzed using Pearson’s-correlation coefficient.@*Results@#(1) There was no significant difference in the percentage of NK cells and in their subpopulations with HBV-related cirrhosis and healthy controls. (2) Siglec-7 expression on NK cells in patients with HBV-related cirrhosis(62.44±13.45%)was significantly down-regulated than that to healthy controls(75.39±12.19%)while the frequency of Siglec-7+ NK cells were negatively correlated with Child-Pugh score. (3) Subpopulation analysis showed that Siglec-7 expression on CD56brightCD16-NK cells(66.99±15.93%)was significantly lower than CD56dimCD16+NK cells(76.54±13.9%) in HBV-related cirrhosis. However, the expression of Siglec-7 in healthy controls showed no difference in these two NK cell subsets. (4) Phenotypic analysis showed that Siglec-7+ NK cells express higher levels of activating receptor CD16, CD38, NKp46 and lower levels of inhibitory receptor CD158b. Indeed, the frequency of CD16 and CD38 on Siglec-7+ NK cells in HBV-related cirrhosis was lower than that in healthy controls.@*Conclusion@#The disease progression in patients with hepatitis B virus-related cirrhosis is associated to decreased frequencies of Siglec-7+NK cells.

Mesenchymal stem cells overexpressing Sirt1 inhibit prostate cancer growth by recruiting natural killer cells and macrophages.

Prostate cancer (PCa) has become the second leading cause of male cancer-related mortality in the United States. Mesenchymal stem cells (MSCs) are able to migrate to tumor tissues, and are thus considered to be novel antitumor carriers. However, due to their immunosuppressive nature, the application of MSCs in PCa therapy remains limited. In this study, we investigated the effect of MSCs overexpressing an NAD-dependent deacetylase sirtuin 1 (MSCs-Sirt1) on prostate tumor growth, and we analyzed the underlying mechanisms. Our results show that MSCs accelerate prostate tumor growth, whereas MSCs-Sirt1 significantly suppresses tumor growth. Natural killer (NK) cells and macrophages are the prominent antitumor effectors of the MSCs-Sirt1-induced antitumor activity. IFN-γ and C-X-C motif chemokine ligand 10 (CXCL10) are highly expressed in MSCs-Sirt1 mice. The antitumor effect of MSCs-Sirt1 is weakened when CXCL10 and IFN-γ are inhibited. These results show that MSCs-Sirt1 can effectively inhibit prostate cancer growthrecruiting NK cells and macrophages in a tumor inflammatory microenvironment.

Changes of number of regulatory T cells and NK cells in tumor tissue and main immune organs of murine models of lung cancer and their significances / 吉林大学学报(医学版)

Objective:To explore the changes of number of CD4+ CD25 + foxp3 + regulatory T cells (Treg)and natural killer cells (NK)in the peripheral immune organs and tumor tissue of the murine models of lung cancer,and to clarify their effects on the development of lung cancer.Methods:The C57BL/6 mice were divided into Lewis lung carcinoma cells (LLC)injection group and normal control group.The mice in LLC injection group were injected with LLC subcutaneously in the armpit to establish the tumor models,while the mice in normal control group were injected with the same amount of saline.The number of CD4+ CD25 + T cells,CD4+ CD25 + foxp3 + Tregs in the spleen,lymph nodes and lung cancer tissues,and the number of NK cells in the spleen tissue were labeled by cell surface or intracellular antibody staining,and detected by flow cytometry.Results:The ratios of CD4+ CD25 + T cells to CD4+ T cells,foxp3+ cells to CD4+ CD25 + T cells,and the number of CD4+ CD25 + foxp3 + Treg in the spleen and lymph nodes of the mice in LLC injection group were increased significantly compared with normal control group (P <0.05 or P <0.01).Moreover,the ratios of CD4+ CD25 + T cells to CD4+ T cells and foxp3 + cells to CD4+ CD25 + T cells in the tumor tissue were significantly higher than those in the spleen and lymph nodes of the mice in LLC injection group.However,the ratio of NK cells in the spleen tissue of the mice in lung cancer group was significantly decreased compared with normal control group (P <0.05).Conclusion:The increase of ratio and the number of Treg cells and the decrease of ratio of NK cells in the main immune organs of lung cancer mice may promote the development of tumor and inhibit the immune response to cancer cells in vivo .

Effect of genetic modified K562 cells on NK cell markers and function / 中国免疫学杂志

Objective:To study the influence of different culture conditions on charcic and inhibition activity of nature killer cells ( NK) ,whether to join the modified K562 cells with IL-6 cytokine.Methods:According to the 5′end of the human IL-6 cDNA sequence,PCR primers designed to amplificate,express and transfect K562 cells cDNA library as a template for DNA.Genetic modified K562 cells as stimulating cells were prepared by expressing IL-6.To extract peripheral blood mononuclear cells( PBMC) from human peripheral blood.PBMC were explanted by genetic modified K562 stimulated.The expansion was initiated by CO-culture of PBMC and irradiate genetic modified K562 cell.The number of NK cell increased by directed induced generation of genetic modified K562 cell.Immunophenotypic analysis of NK cell surface markers was performed by flow cytometry (FCM).51Cr release assay was employed to measure the specific lysis skilling of NK cell target K562 cells.Results:We have constracted genetic modified K562 cells by genetic engineering.As stimulated cell added into the PBMC,an average of 760 ±18 fold expansion of CD56+CD16+CD3-cells was observed after 3 weeks of co-culture system.The NK cells population could proliferated more 91%±2% after expansion comparing with 6%± 0.4%in PBMC before expansion by FCM.The cytotoxical activity of NK cells which was induced by genetic modified K562 cell was the strongest than induced by IL-6 cytokine alone.The expanded NK cells lysed 92%±2% of K562 targets in a 5∶1 effector to target ratio.In this case,the NK cells induced by genetic modified K562 cells against tumor cells was more lethal.Conclusion:PBMC based in vitro expansion of natural killer cells was set up by genetic modified K562 cells.The cytotoxicity of NK cells was the strongest induced by genetic modified K562 cell treated.These results had important guiding significance for the the NK large number of amplification and used in clinical.

Gender-specific immunological effects of the phosphodiesterase 5 inhibitor sildenafil in healthy mice.

Phosphodiesterase 5 (PDE5) is a pharmacological target in erectile dysfunction, pulmonary hypertension and in other indications. In tumor-bearing mice an inhibition of PDE5 with sildenafil prolongs survival of the animals through the augmentation of antitumor immunity, indicating the immunomodulatory properties of this drug. Effects of sildenafil on the immune system in healthy organisms are poorly investigated. In this work we showed that chronic application of sildenafil in healthy mice leads to opposite gender-dependent effects on NK cells, subpopulations of CD4(+) and CD8(+) T cells, activated conventional T cells, and to a decrease in Gr-1(+)CD11b(+) immature myeloid cells. Besides, sildenafil treatment decreases the serum concentration of interleukin-6. Ex vivo cultivation of isolated splenocytes with sildenafil results in an increase in CD4(+) T cells and a concomitant decrease in B cells and central memory CD8(+) T cells. Ex vivo modulatory properties of sildenafil are not gender-specific, indicating the importance of sildenafil's pharmacokinetics for it immunomodulatory activity in vivo. While the PDE5 expression is equal in the splenocytes from both genders, splenocytes from female mice possess higher basal level of cGMP compared to the male ones. Moreover, cultivation of splenocytes obtained from female but not male mice with sildenafil leads to an increase in cGMP concentration, making sildenafil's pharmacodynamics also responsible for gender-specific effects of the drug. Thus, this work secures conclusive evidence that the PDE5 inhibitor sildenafil possesses immunomodulatory properties and these effects are gender-specific. Immunological clinical trials are needed to prove the potential immunomodulatory effects of sildenafil in humans.

The regulating function of nature killer cells in immune system / 国际儿科学杂志

Nature killer ( NK) cells, important innate immune cells, can respond in an antigenindependent manner as well as secrete huge amounts of cytokines, which can regulate acquired immunity. The role of NK cells in immune system attracts increasingly attention. Resent studies have shown that the regulating function of NK cells is by reacting with dendritic cells and secreting cytokines.

Effects of Grifola frondosa extracts on mouse immunity / 中国免疫学杂志

Objective :To investigate the effects of ethanol precipitate(ET-Pre) and RNA of Grifola frondosa on non-specific immunity in mouse.Methods:The common biological methods were used to examine the levels of cytokines and immunocyte activity. Results: The killing activity of the NK cells, the phagocytosis function of macrophages and the levels of TNF?/IL-1 in the animals treated with ET-Pre and RNA respectively were significantly higher than those in the control.The RNA was stronger than ET-Pre in increasing killing activity of NK cells and phagocytosis function of macrophages. Conclusion:Both ET-Pre and RNA extracts of Grifola frondosa may promote immunoactivity nonspecifi-cally and inhibit tumor cells indirectly.