ABSTRACT
With the deeper understanding of tumor , more and more evidence indicates that the occurrence and development of tumors are closely related to the body′s immune function .More and more researches focus on tumor immunology to find an effective way of enhancing anti-tumor immunity . Radiotherapy has played an important role in anti-tumor immunity recently though it was believed as a traditional treatment for cancer before .Radiotherapy could convert a cold tumor into a hot tumor, which might ameliorate immune suppressive microenvironment , improve tumor immunogenicity and activate the cellular immune response .However, the abscopal effectof single radiotherapy is very rare . Immunotherapy is capable of enhancing the immune response produced by radiotherapy .In this paper , the basic theory and clinical practice of radiotherapy and immunotherapy were reviewed and the related clinical strategies were summarized .
ABSTRACT
Radiotherapy ( RT) is used as primary treatment for numerous cancers. Although it is usually described as an immunosuppressive modality,there are new preclinical evidences suggesting that RT could have also generated substantial changes in the tumor microenvironment, including triggering an inflammatory process. Some studies established the proof of concept that combining RT with strategies modifying immunology could enhance antitumor effects.
ABSTRACT
Radiotherapy ( RT) is used as primary treatment for numerous cancers. Although it is usually described as an immunosuppressive modality,there are new preclinical evidences suggesting that RT could have also generated substantial changes in the tumor microenvironment, including triggering an inflammatory process. Some studies established the proof of concept that combining RT with strategies modifying immunology could enhance antitumor effects.
ABSTRACT
In recent years, the immunotherapy based on the blocking of programmed death-1 (PD-1)/programmed death-ligand 1 (PD-L1) pathway has achieved encouraging progress in the treatment of malignant tumors such as melanoma and lung cancer. More and more studies have focused on its role in hepatocellular carcinoma (HCC). This article introduces the mechanism of action of PD-1/PD-L1, expression of PD-L1 in HCC tissues, and its basic and clinical research in the treatment of HCC, and points out that PD-L1 plays an important role in tumor immune escape and is expected to become an independent index for evaluating the prognosis of HCC. The discovery of PD-1/PD-L1 pathway provides a new target for immunotherapy for HCC.
ABSTRACT
Objective:To explore the influence on inflammation cytokines for anti-IL-1βand TNF-αIgY intranasal treatment in guinea pigs with allergic rhinitis.Methods:The allergic rhinitis model in guinea pigs was established using ovalbumin(OVA).Hartley guinea pigs were randomly divided into the control group(group C,n=17),the allergic rhinitis model group(group M,n=27),the 0.1%anti-IL-1βand TNF-αIgY treatment group(group Z1,n=21)and the fluticasone propionate treatment group(group Z2,n=21). At 2 h,4 h and 8 h after the last treatment,blood was got by heart puncture,as well as nose was lavaged using 0.9% saline and the nasal lavage fluid( NLF) was collected.The level of cytokines was examined using ELISA kits.Results: In the peripheral blood, the levels of IL-1β,IL-5,IL-9,IL-13,IL-18,IL-33 and TGF-β1 from 2 h to 8 h;TNF-αand OVA-specific IgE from 2 h to 4 h;and IL-22 from 4 h to 8 h were significantly decreased in the 0.1%anti-IL-1βand TNF-αIgY treatment group compared with the allergic rhinitis model group(P<0.05).In the NLF,the levels of IL-1β,IL-5,IL-9,IL-13,IL-22,IL-33,TNF-α,TGF-β1 and OVA-specific IgE from 2 h to 8 h;and IL-18 at 2 h were significantly decreased in the 0.1% anti-IL-1βand TNF-αIgY treatment group compared with the allergic rhinitis model group ( P<0.05 ) .Conclusion: Anti-IL-1βand TNF-αIgY intranasal treatment can significantly reduce inflammation cytokine levels in allergic rhinitis guinea pigs.
ABSTRACT
Objective:To investigate therapeutic mechanism of immunoglobulin Yolk (IgY) against tumour necrosis factor alpha ( TNF-α) and interleukin-1 beta ( IL-1β) in guinea pigs with allergic rhinitis.Methods: Hartley guinea pigs were randomly divided into the control group (group C,n=17),the allergic rhinitis model group (group M,n=27),the 0.1%anti-TNF-αand IL-1βIgY treating group (group Z1,n=21) and the fluticasone propionate treating group (group Z2,n=21).The allergic rhinitis model in guinea pigs was established using ovalbumin.After treatment for 2 h,4 h,8 h,nose and bronchial lung were lavaged using 0.9%saline, the nasal lavage fluid (NLF) and bronchoalveolar lavage fluid (BALF) were collected,the precipitated cells were stained using Wright′s,the nasal mucosa and lung tissues were stained using methylene blue and eosin (HE),and TNF-α,IL-1β,IL-5 and IL-33 in nasal mucosa and lung tissues were stained using immunohistochemistry.Results:There were a large amount of eosinophils and more serious inflammation responses in nasal mucosa in the M group compared with the Z 1 and Z2 groups.In the lung tissues,there were more alveolar tube damage ,pulmonary interstitial edema ,interval thickening ,thickening of bronchial smooth muscle and inflammation cell in-filtration in the M group compared with the Z 1 and Z2 groups.The eosinophils ,lymphocytes and neutrophils were significantly decreased in NLF and BALF in the Z1 and Z2 groups compared with the M group (P<0.05).The expressions of IL-1βand TNF-αfrom 2 h to 8 h and IL-5 and IL-33 from 4 h to 8 h significantly decreased in the nasal mucosa and lung tissues in the Z 1 group compared with the M group ( P<0.05 ).Conclusion:The allergic rhinitis in guinea pigs accompany with the allergic asthma.The inhibitory capacity of anti-TNF-αand IL-1βIgY on pathological responses in guinea pigs with allergic rhinitis may be due to the significant decrease in the infiltration of eosinophils and the expressions of inflammatory cytokines in the nasal mucosas and lung tissues .
ABSTRACT
Objective To analyze the relationship between the expression of formlin-like 2(FMNL2)and colorectal carcinoma metastasis through the detection of the expression of FMNL2 in colorectal carcinoma tissue and paracancerous tissue.Methods ①Immunohistochemistry was used to detect the expression of FMNL2 in 175 cases of paraffin wax specimens(including 30 cases of normal mucosa,25 cases of adenoma,75 cases of colorectal carcinoma and 45 cases of metastatic tumors).②Real time-PCR was used to detect FMNL2 mRNA expression in 32 cases of fresh specimens of carcinoma and 32 cases of paracancerous tissue.Results The positive detection rate of FMNL2 was higher in colorectal carcinoma tissue than in paracancerous tissue(P=0.003),higher in lymphatic metastasis than in primary carcinoma tissue(P=0.037),and was aslo higher in metastatic carcinoma tissue than in non metastatic carcinoma tissue(P=0.011).The expression of FMNL2 mRNA was not related to the infiltration and differentiation of carcinoma tissue but its concentration in metastatic carcinoma tissue was 2.5 times higher than in non metastatic carcinoma tissue.Conclusion FMNL2 gene may play an important role in the metastasis of colorectal carcinoma.
ABSTRACT
Objective To construct the specific small hairpin RNA(shRNA)plasmids for Formin-like 2(FMNL2)gene,and to observe its effect on proliferation of SW620.Methods Plasmids FMNL21 shRNA and plasmids FMNL22 shRNA complimentary to the sequence responsible for the function domain of human FMNL2 were constructed and transfected into SW620,respectively.The inhibition rates of FMNL2 expression were detected by re-al-time PCR after transfection with PGenesil-FMNL21 and PGenesil-FMNL22,respectively.The expression of FMNL2 was detected by real-time PCR at 12,24,48,72 and 96h after transfection.At 48 h and 72 h after transfection,the proliferation of SW620 was detected using MTT assay.Resuits The transfection rate in SW620 was(60.8±2.8)%for PGenesil-FMNL21,(58.7±2.9)%for PGenesil-FMNL22,and(62.6±1.7)%for PGenesil-HK(P＞0.05).The inhibition rate of FMNL2 expression after transfection with PGenesil-FMNL21 was 77.1%,which was the highest.The inhibition rates of FMNL2 expression were 13.5%,57.3%,80.3%,62.4%,and 33.2%at 12,24,48,72and 96h after transfection respectively.The proliferat capability of SW620 was obviously lower than that of control cells(P＜0.05).Conclusion Both plasmids FMNL21 shRNA and plasmids FMNL22 shRNA can inhibit the expression of FMNL2,of which Pgenesil-FMNL21 execs the greatest role.FMNL2 could be related to the proliferation of SW620.
ABSTRACT
Objective To investigate the effect of atorvastain on plasma levels of nitric oxide(NO) and alpha-granule membrance protein-140(GMP-140) in patients with acute cerebral infarction.Methods 94 cases with acute cerebral infarction were randomly divided into the atorvastain group(48 cases) and the control group(46 cases).Plasma NO and GMP-140 were determined by the method of nitrate reductase and enzyme-linked immunosorbent assay in atorvastain group and control group at moment of hospitalization and after four weeks.Results Plasma NO and GMP-140 of atorvastain group after treatment were statistically lower than that of controls(P0.05).Conclusion Atorvastain can reduce plasma levels of NO and GMP-140 in patients with acute cerebral infarction.It can ameliorate brain injury after ischemia and has protective effect on the ischemia cerebral tissue.