Regulatory T cells(Tregs)are key regulators of the immune system and play important roles intumorigenesis and tumor progres-sion.They exert immunosuppressive effects through immune checkpoint pathways and by secreting inhibitory cytokines and specific chemokines as well as through other mechanisms that promote tumor immune escape.However,their mechanisms of action are complex and involve multistage,multifactorial processes.This article summarizes the mechanisms by which Tregs exert immunosuppressive effects in tumors and promote immune escape and describes related research progress.This study aims to provide a reference for an indepth under-standing of immune regulatory mechanisms in tumors and the development of novel therapeutic strategies.

Regulatory T cells(Tregs)are key regulators of the immune system and play important roles intumorigenesis and tumor progres-sion.They exert immunosuppressive effects through immune checkpoint pathways and by secreting inhibitory cytokines and specific chemokines as well as through other mechanisms that promote tumor immune escape.However,their mechanisms of action are complex and involve multistage,multifactorial processes.This article summarizes the mechanisms by which Tregs exert immunosuppressive effects in tumors and promote immune escape and describes related research progress.This study aims to provide a reference for an indepth under-standing of immune regulatory mechanisms in tumors and the development of novel therapeutic strategies.

Objective To investigate serum adiponectin level in patients with Alzheimer's disease (AD) and its correlation with the patients' cognitive function. Methods This case-control study was conducted in 90 patients with a highly probable diagnosis ofAD, who were divided into mild, moderate and severe group saccording to the MMSE score. Ninety healthy subjects matched for age and gender with the AD patients were selected as the control group. The serum levels ofadiponectin in the participants were detected using enzyme-linked immunosorbent assay. Results Serum adiponectin level was significantly lower in the AD group than in the control group (P<0.05). Of the 3 subgroups of the AD patients, the moderate and severe AD groups showed significantly lower serum adiponectin level sthan the control group (P<0.05), but the difference in adiponectin levels was not significant between the mild AD group and the control group (P>0.05);serum adiponectin levels also differed significantly among the 3 subgroups of AD patients (P<0.05). Serum adiponectin level was positively correlated with the MMSE score in the AD patients (r=0.683, P<0.001). Conclusion Serum adiponectin levels are reduced in AD patients and associated with the degree of cognitive impairment.

Objective To investigate serum adiponectin level in patients with Alzheimer's disease (AD) and its correlation with the patients' cognitive function. Methods This case-control study was conducted in 90 patients with a highly probable diagnosis ofAD, who were divided into mild, moderate and severe group saccording to the MMSE score. Ninety healthy subjects matched for age and gender with the AD patients were selected as the control group. The serum levels ofadiponectin in the participants were detected using enzyme-linked immunosorbent assay. Results Serum adiponectin level was significantly lower in the AD group than in the control group (P<0.05). Of the 3 subgroups of the AD patients, the moderate and severe AD groups showed significantly lower serum adiponectin level sthan the control group (P<0.05), but the difference in adiponectin levels was not significant between the mild AD group and the control group (P>0.05);serum adiponectin levels also differed significantly among the 3 subgroups of AD patients (P<0.05). Serum adiponectin level was positively correlated with the MMSE score in the AD patients (r=0.683, P<0.001). Conclusion Serum adiponectin levels are reduced in AD patients and associated with the degree of cognitive impairment.

OBJECTIVETo determine the association between the polymorphism of angiotensin converting enzyme (ACE) gene and Alzheimer's disease (AD).

METHODSThis case-control study involved 201 AD patients and 257 healthy subjects matched for age and gender as the control group. Polymerase chain reaction amplification and matrix-assisted laser desorption/ ionization time of flight mass spectrometry were used to examine the rs4291, rs4309, and rs4343 of ACE gene, and the difference in genotypes, allelotype frequencies and haplotype frequencies were analyzed between the two groups.

RESULTSNo statistic difference was found in the genotype and allelotype frequencies of rs4291 locus between AD and control groups (P>0.05). A significant difference was found in the genotype and allelotype frequencies of rs4309 between the two groups with a significant increase in the C allelotype frequency in AD group (OR=1.917, 95% CI=1.431-2.568, P<0.05). The difference in the genotype frequency of rs4343 was not significant between the two groups, but the allelotype frequencies differed significantly with a decreased A allelotype frequency in AD group(OR=0.714, 95% CI=0.532-0.957, P=0.024). Analysis of the linkage disequilibrium among the loci of rs4291, rs4309 and rs4343 showed a D' all above 0.65 between one another. Haplotype analysis confirmed the existence of 5 haplotypes, namely ATA, ACA, TCA, TCG and TTG, indicating a negative correlation between haplotype ATA and AD occurrence (OR=0.558, 95% CI=0.420-0.741, P<0.05) and positive correlations of haplotype ACA and TCA with AD occurrence (ACA: OR=4.883, 95% CI=2.267-10.518, P<0.05; TCA: OR=2.269, 95% CI=1.083-4.754, P<0.05).

CONCLUSIONThe polymorphism of rs4291 may have no relation with the incidence of AD. Polymorphisms of s4309 and rs4343 may be related to AD, and ATA, ACA and TCA haplotypes composed of rs4291/rs4309/rs4343 may be related to AD.

Alzheimer Disease ; genetics ; Case-Control Studies ; Gene Frequency ; Genotype ; Haplotypes ; Humans ; Linkage Disequilibrium ; Peptidyl-Dipeptidase A ; genetics ; Polymorphism, Single Nucleotide

Objective To determine the association between the polymorphism of angiotensin converting enzyme (ACE) gene and Alzheimer's disease (AD). Methods This case-control study involved 201 AD patients and 257 healthy subjects matched for age and gender as the control group. Polymerase chain reaction amplification and matrix-assisted laser desorption/ionization time of flight mass spectrometry were used to examine the rs4291, rs4309, and rs4343 of ACE gene, and the difference in genotypes, allelotype frequencies and haplotype frequencies were analyzed between the two groups. Results No statistic difference was found in the genotype and allelotype frequencies of rs4291 locus between AD and control groups (P>0.05). A significant difference was found in the genotype and allelotype frequencies of rs4309 between the two groups with a significant increase in the C allelotype frequency in AD group (OR=1.917, 95% CI=1.431-2.568, P<0.05). The difference in the genotype frequency of rs4343 was not significant between the two groups, but the allelotype frequencies differed significantly with a decreased A allelotype frequency in AD group(OR=0.714, 95%CI=0.532-0.957, P=0.024). Analysis of the linkage disequilibrium among the loci of rs4291, rs4309 and rs4343 showed a D’all above 0.65 between one another. Haplotype analysis confirmed the existence of 5 haplotypes, namely ATA, ACA, TCA, TCG and TTG, indicating a negative correlation between haplotype ATA and AD occurrence (OR=0.558, 95% CI=0.420-0.741, P<0.05) and positive correlations of haplotype ACA and TCA with AD occurrence (ACA:OR=4.883, 95%CI=2.267-10.518, P<0.05;TCA:OR=2.269, 95%CI=1.083-4.754, P<0.05). Conclusion The polymorphism of rs4291 may have no relation with the incidence of AD. Polymorphisms of s4309 and rs4343 may be related to AD, and ATA, ACA and TCA haplotypes composed of rs4291/rs4309/rs4343 may be related to AD.

Objective To determine the association between the polymorphism of angiotensin converting enzyme (ACE) gene and Alzheimer's disease (AD). Methods This case-control study involved 201 AD patients and 257 healthy subjects matched for age and gender as the control group. Polymerase chain reaction amplification and matrix-assisted laser desorption/ionization time of flight mass spectrometry were used to examine the rs4291, rs4309, and rs4343 of ACE gene, and the difference in genotypes, allelotype frequencies and haplotype frequencies were analyzed between the two groups. Results No statistic difference was found in the genotype and allelotype frequencies of rs4291 locus between AD and control groups (P>0.05). A significant difference was found in the genotype and allelotype frequencies of rs4309 between the two groups with a significant increase in the C allelotype frequency in AD group (OR=1.917, 95% CI=1.431-2.568, P<0.05). The difference in the genotype frequency of rs4343 was not significant between the two groups, but the allelotype frequencies differed significantly with a decreased A allelotype frequency in AD group(OR=0.714, 95%CI=0.532-0.957, P=0.024). Analysis of the linkage disequilibrium among the loci of rs4291, rs4309 and rs4343 showed a D’all above 0.65 between one another. Haplotype analysis confirmed the existence of 5 haplotypes, namely ATA, ACA, TCA, TCG and TTG, indicating a negative correlation between haplotype ATA and AD occurrence (OR=0.558, 95% CI=0.420-0.741, P<0.05) and positive correlations of haplotype ACA and TCA with AD occurrence (ACA:OR=4.883, 95%CI=2.267-10.518, P<0.05;TCA:OR=2.269, 95%CI=1.083-4.754, P<0.05). Conclusion The polymorphism of rs4291 may have no relation with the incidence of AD. Polymorphisms of s4309 and rs4343 may be related to AD, and ATA, ACA and TCA haplotypes composed of rs4291/rs4309/rs4343 may be related to AD.

OBJECTIVETo investigate the presence of β-amyloid peptide (Aβ) deposition in the cerebellum and the expression of related miRNAs in the cerebellum of a mouse model of Alzheimer disease.

METHODSTwelve 12-month-old APPswe/PSδE9 double transgenic mice and 12 wild-type C57 mice were sacrificed and the brain tissues were taken for examination. The right hemisphere was stained with Congo red to observe the deposition of amyloid substances, and from the left hemisphere, the hippocampus and the cerebellum were dissected for detecting the expression of miRNA-135a-5p, miRNA-298-5p, miRNA-466b-3p and miR-669f-3p using real-time PCR.

RESULTSCongo red staining revealed the presence of Aβ deposition in both the hippocampus and the cerebellum of the transgenic mice but not in the control mice. Real-time PCR showed a significantly lower expression of the 4 miRNAs in the hippocampus in the transgenic mice than in the control mice (P<0.05). The expression of miRNA-135a-5p, miRNA-298-5p, and miR-669f-3p in the cerebellum was significantly lower in the transgenic mice than in the control mice (P<0.05). The expression of miRNA-298-5p and miR-669f-3p in the hippocampus was significantly lower than that in the cerebellum of the transgenic mice (P<0.05).

CONCLUSIONβ deposition also occurs in the cerebellum of APPswe/PSδE9 double transgenic mice, and its formation might be related to the down-regulation of miRNA-135a-5p, miRNA-298-5p, and miR-669f-3p.

Alzheimer Disease ; metabolism ; Amyloid beta-Peptides ; metabolism ; Animals ; Cerebellum ; metabolism ; Disease Models, Animal ; Hippocampus ; metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; MicroRNAs ; metabolism

Objective To investigate the presence of β-amyloid peptide (Aβ) deposition in the cerebellum and the expression of related miRNAs in the cerebellum of a mouse model of Alzheimer disease. Methods Twelve 12-month-old APPswe/PS△E9 double transgenic mice and 12 wild-type C57 mice were sacrificed and the brain tissues were taken for examination. The right hemisphere was stained with Congo red to observe the deposition of amyloid substances, and from the left hemisphere, the hippocampus and the cerebellum were dissected for detecting the expression of miRNA-135a-5p, miRNA-298-5p, miRNA-466b-3p and miR-669f-3p using real-time PCR. Results Congo red staining revealed the presence of Aβdeposition in both the hippocampus and the cerebellum of the transgenic mice but not in the control mice. Real-time PCR showed a significantly lower expression of the 4 miRNAs in the hippocampus in the transgenic mice than in the control mice (P<0.05). The expression of miRNA-135a-5p, miRNA-298-5p, and miR-669f-3p in the cerebellum was significantly lower in the transgenic mice than in the control mice (P<0.05). The expression of miRNA-298-5p and miR-669f-3p in the hippocampus was significantly lower than that in the cerebellum of the transgenic mice (P<0.05). Conclusion Aβdeposition also occurs in the cerebellum of APPswe/PS△E9 double transgenic mice, and its formation might be related to the down-regulation of miRNA-135a-5p, miRNA-298-5p, and miR-669f-3p.

Objective To investigate the presence of β-amyloid peptide (Aβ) deposition in the cerebellum and the expression of related miRNAs in the cerebellum of a mouse model of Alzheimer disease. Methods Twelve 12-month-old APPswe/PS△E9 double transgenic mice and 12 wild-type C57 mice were sacrificed and the brain tissues were taken for examination. The right hemisphere was stained with Congo red to observe the deposition of amyloid substances, and from the left hemisphere, the hippocampus and the cerebellum were dissected for detecting the expression of miRNA-135a-5p, miRNA-298-5p, miRNA-466b-3p and miR-669f-3p using real-time PCR. Results Congo red staining revealed the presence of Aβdeposition in both the hippocampus and the cerebellum of the transgenic mice but not in the control mice. Real-time PCR showed a significantly lower expression of the 4 miRNAs in the hippocampus in the transgenic mice than in the control mice (P<0.05). The expression of miRNA-135a-5p, miRNA-298-5p, and miR-669f-3p in the cerebellum was significantly lower in the transgenic mice than in the control mice (P<0.05). The expression of miRNA-298-5p and miR-669f-3p in the hippocampus was significantly lower than that in the cerebellum of the transgenic mice (P<0.05). Conclusion Aβdeposition also occurs in the cerebellum of APPswe/PS△E9 double transgenic mice, and its formation might be related to the down-regulation of miRNA-135a-5p, miRNA-298-5p, and miR-669f-3p.