CCL2 Research Articles

Solution structure of CCL2 in complex

Solution structure of CCL2 in complex

Effects of γ-ray total body irradiation from a 60Co source on expression level of intrathymic forkhead box protein N1 in mice

Effects of γ-ray total body irradiation from a 60Co source on expression level of intrathymic forkhead box protein N1 in mice

ChemInform Abstract: The Dimerization of Thiophosgene and Trichlorothioacetyl Chloride S‐Imides — Head‐to‐Head and/or Head‐to‐Tail?

AbstractReview: 31 refs.

Inhibition of CCL2 dependent human cytomegalovirus replication by tricin

Inhibition of CCL2 dependent human cytomegalovirus replication by tricin

GPI-anchored CCL28 as a strong mucosal immunostimulator with influenza VLPs

GPI-anchored CCL28 as a strong mucosal immunostimulator with influenza VLPs

The dimerization of thiophosgene and trichlorothioacetyl chloride S-imides – Head-to-head and/or head-to-tail?

GRAPHICAL ABSTRACT

CCL22/CCR4 signaling induces immune escape in hepatocellular carcinoma

Objective To investigate the regulation of CCL22/CCR4 signaling on CD4+ CD25+ regulatory T cells (Tregs) and immune escape in hepatocellular carcinoma (HCC). Methods CCL22, interleukin-2 (IL-2), transforming growth factor-β (TGF-β), and interleukin-10 (IL-10) levels in tumor tissue of 30 HCC patients were determined by ELISA. Tumor infiltrating lymphocytes were isolated and assayed by flow cytometry to evaluate the change of CD4+ CD25+ Tregs in tumor tissue, and CCR4 in CD4+ CD25+ Tregs were detected. Results The CCL22 level in tumor tissue was obviously increased. The level of CCL22 in tumor tissue was (920.1±180.1)ng/L, which was significantly higher than that in non-tumor tissue[(227.2±108.6) ng/L; P<0.05]. The tumor infiltrating CD4+ CD25+ Tregs was obviously increased, reaching approximately to (13.3±4.0)%, and the CCR4 expression in CD4+ CD25+ Tregs increased to (8.8±3.0)%. Along with progression in clinical TNM staging, the levels of CD4+ CD25+ Tregs and CD4+ CD25+ CCR4+ Tregs in tumor tissue increased, and were correlated with the CCL22 level. IL-2 level in tumor tissue was decreased, but TGF-β and IL-10 levels were increased. HCC tissue can secrete a large amount of CCL22 that could recruit CD4+ CD25+ Tregs to tumor tissue by activating CCL22/CCR4 signaling. CD4+ CD25+ Tregs played an important role in the immune escape of HCC by releasing plenty of TGF-β and IL-10 and inhibiting IL-2 secretion. Conclusion This study validates CCL22/CCR4 as therapeutic targets in immunotherapy for HCC. Key words: Hepatocellular carcinoma; Regulatory T cells; Immune escape

Investigation of the association of ccl22 gene polymorphism rs4359426 with multiple sclerosis

Background: CCL22 is a chemokine that induces the migration of Th2- and regulatory T cells to the inflammatory sites. The aim of this study was to investigate the association of a single nucleotide polymorphism (SNP), rs4359426, in CCL22 gene, with multiple sclerosis (MS) in patients from southeast of Iran. Materials and Methods: The blood samples collected from 150 patients with MS and 150 healthy subjects as a control group. The serum levels of CCL20 measured by ELISA and the DNA analyzed for CCL22 polymorphism using PCR-RFLP method. Results: There were no significant differences in the frequencies of genotypes and alleles at SNP rs4359426 in CCL22 gene between MS patients and controls. No significant differences also observed between controls and patients with RRMS, SPMS, PPMS and PRMS patterns regarding the genetic variation of rs4359426. In both MS and control groups, no significant differences were observed between subjects with CC, CA and AA genotypes or between subjects with C and A alleles concerning rs4359426 with respect to the serum levels of CCL22. Conclusion: These results do not show any association between the investigated genotypes and alleles at rs4359426 in CCL22 gene with MS or its patterns in MS patients. The serum levels of chemokine did not also influence by genetic variation of SNP rs4359426.

Molecular expression analysis of different inflammatory mediators and their role in breast cancer progression and metastasis

Introduction: Cytokines include different subfamilies such as interleukins (IL), chemokines, and growth factors. They play an important role in inflammatory conditions such as cancer progression and metastasis. There is an increasing interest in developing strategies to antagonize the function of some cytokine/chemokine to interfere with tumor progression and metastasis, the leading cause of death in most patients. The aim of the research project is to study the molecular characteristics of a sample of Syrian patients with breast cancer and assess the protein and gene expression of different inflammatory mediators and correlate that with the clinicopathological criteria of tumors. Materials and methods: Patient samples will be evaluated histologically (H&E stain) and stained immunohistochemically with antibodies against important molecular markers, cytokines, and different types of activated leukocytes. Immunohistochemistry of CD206, a marker of alternatively activated macrophages in tumors is shown here. PCR and immunohistochemical analysis of cytokines (e.g. IL-2, GM-CSF, IFNγ, M-CSG, IL-4, IL-10, CXCL8, CXCL12, CCL21, CCL19, CCR7) will be further implemented. The staining intensity, localization and distribution within the tumor will be examined and correlated with the gene expression and other clinnicopathological information. Expected results: We expect to get new information about the role of different cytokines in breast cancer progression in addition to get an insight into the possible inter-relationship between these cytokines.

Effects of rottlerin on in vitro proliferation of and expressions of interleukin-17C, CCL20 and nuclear factor-κB in a human keratinocyte cell line HaCaT

Objective To investigate the effects of rottlerin on in vitro proliferation of and expressions of interleukin (IL) - 17C, CCL20 chemokine, and nuclear factor (NF) - κB in cultured human HaCaT keratinocytes. Methods Some HaCaT cells were divided into several test groups treated with rottlerin at concentrations of 0.5, 1.0, 2.0 and 4.0 μmol/L, a solvent group treated with RPMI 1640 culture solution containing the same volume of dimethyl sulfoxide (DMSO) as that of 4.0 μmol/L rottlerin, and a control group treated with RPMI 1640 culture solution. Cell counting kit-8 (CCK8) assay was conducted to estimate the proliferative activity of HaCaT cells after 24-, 48- and 72-hour culture, RT-PCR to determine the mRNA expressions of IL-17C and CCL20 after 48-hour culture, and Western blot to measure the protein expressions of IL-17C, CCL20 and NF-κB after 48-hour culture. Statistical analysis was carried out by using repeated-measures analysis of variance, one-way analysis of variance and Pearson correlation analysis with the SPSS16.0 software. Results Rottlerin showed an inhibitory effect on the proliferation of HaCaT cells, and the inhibitory effect increased over time (F=126.936, P < 0.05) and with the increase of rottlerin concentrations (F=838.308, P < 0.05), with a significant interaction effect between rottlerin concentrations and treatment duration (F=15.961, P < 0.05). After 48-hour treatment, a significant decrease was observed in the mRNA and protein expressions of IL-17C (F=206.041, 233.887, respectively, both P < 0.05) and CCL20 (F=143.883, 162.431, respectively, both P < 0.05), as well as in the protein expression of NF-κB (F=577.915, P < 0.05) in the test groups with the increase in rottlerin concentrations. Conclusions Rottlerin can inhibit the proliferation of HaCaT cells in vitro, and decrease the mRNA and protein expressions of IL-17C and CCL20 likely by downregulating the protein expression of NF-κB. Key words: Keratinocytes; Cell proliferation; NF-kappa B; Interleukin-17; Chemokine CCL20; Psoriasis; HaCaT cells; Rottlerin

Role of spinal MCP-1-ERK-KIF17/NR2B signaling pathway in maintenance of type 2 diabetic neuropathic pain in rats

Objective To explore the role of spinal monocyte chemoattractant protein-1 (MCP-1) -extracellular signal-regulated protein kinase (ERK) -kinesin superfamily motor protein 17 (KIF17) /N-methyl-D-aspartate receptor subunit 2B (NR2B) signaling pathway in the maintenance of type 2 diabetic neuropathic pain (DNP) in rats. Methods Type 2 diabetes mellitus was induced by a high-fat and high-sucrose diet and intraperitoneal streptozotocin (STZ) 35 mg/kg, and confirmed by fasting blood glucose level≥16.7 mmol/L 3 days later in male Sprague-Dawley rats aged 6 weeks.Type 2 DNP was confirmed when the mechanical paw withdrawal threshold (MWT) and thermal paw withdrawl latency (TWL) measured on day 14 after STZ administration decreased to < 80% of the baseline value.The rats with type 2 DNP were randomly divided into 4 groups (n=36 each) using a random number table: type 2 DNP group (group DNP) , type 2 DNP + MCP-1 neutralizing antibody group (group DM) , type 2 DNP + ERK inhibitor group (group DE) and type 2 DNP + dimethyl sulfoxide group (group DD) . In DM, DE and DD groups, 0.1 ng/μl MCP-1 neutralizing antibody 10 μl, 0.5 μg/μl U0126 10 μl and 5 % dimethyl sulfoxide 10 μl were injected intrathecally, respectively, once a day for 14 consecutive days starting from 14 days after administration of STZ.Another 36 normal rats fed a common forage diet were adopted as control group (group C) . MWT and TWL were measured before STZ injection and at 1, 3, 7 and 14 days after STZ injection (T0-4) . Nine rats were sacrificed after measurement of pain thresholds at T1-4, and the lumbar segments (L4-6) of the spinal cord were removed for determination of the expression of phosphorylated ERK (p-ERK) , KIF17 and phosphorylated NR2B (p-NR2B) by Western blot. Results Compared with group C, the MWT was significantly decreased, the TWL was shortened, and the expression of p-ERK, KIF17 and p-NR2B was up-regulated at T1-4 in DNP, DM, DE and DD groups.Compared with group DNP, the MWT at T3-4 in group DM and at T2-4 in group DE was significantly increased, the TWL at T3-4 in group DM and at T2-4 in group DE was prolonged, and the expression of p-ERK, KIF17 and p-NR2B was down-regulated at T2-4 in DM and DE groups, and no significant changes were found in the parameters mentioned above in group DD. Conclusion Spinal MCP-1-ERK-KIF17/NR2B signaling pathway is involved in the maintenance of type 2 DNP in rats. Key words: Diabetes mellitus, type 2; Neuropathic pain; Chemokine CCL2; Extracellular Signal-Regulated MAP Kinases; Receptors, N-Methyl-D-Aspartate; Kinesin; Spinal cord

Relationship between hippocampal monocyte chemotactic protein-1 and its receptor and postoperative cognitive dysfunction in aged rats

Objective To evaluate the relationship between hippocampal monocyte chemotactic protein-1(MCP-1)and its receptor C-C chemokine receptor 2(CCR2)and postoperative cognitive dysfunction(POCD)in aged rats. Methods Forty-eight male Sprague-Dawley rats, aged 20-22 months, weighing 480-550 g, were randomly divided into 2 groups(n=24 each)using a random number table: control group(group C)and POCD group.POCD group inhaled 2.0% isoflurane and underwent splenectomy.Before surgery and at 1, 3 and 7 days after surgery, Morris water maze test was performed to evaluate the spatial learning and memory ability.The escape latency and swimming distance were recorded.Eight rats were sacrificed after the end of Morris water maze test performed at 1, 3 and 7 days after surgery.Then the brains were removed, and the hippocampi were isolated for detection of the expression of MCP-1 and CCR2 by Western blot. Results Compared with group C, the escape latency and swimming distance were significantly prolonged, and the expression of MCP-1 and CCR2 in hippocampi was up-regulated at 1, 3 and 7 days after surgery in POCD group. Conclusion Up-regulation of hippocampal MCP-1 and CCR2 expression may be involved in the mechanism of POCD in aged rats. Key words: Chemokine CCL2; Receptors, CCR2; Hippocampus; Aged; Cognition disorders; Postoperative complications

The correlation between human chemokine type 1 chemokine ligand 3 and chemokine ligand 4 gene and the immune reconstitution of acquired immunodeficiency syndrome patients after antiretroviral therapy

Objective To investigate the correlation between the human chemokine type 1 chemokine ligand 3 (CCL3L1) and chemokine ligand 4 (CCL4L) gene expression and the immune reconstitution of acquired immunodeficiency syndrome (AIDS) patients after antiretroviral therapy. Methods The gene copy numbers of CCL3L1 and CCL4L were detected by real time polymerase chain reaction in 217 AIDS patients before antiretroviral therapy. And the correlation between CCL3L1 and CCL4L gene copy numbers and the level of CD4+ and CD8+ T lymphocytes were analyzed. The changes of CD4+ and CD8+ T lymphocytes were defined as mean change value per month after 48 months treatment. The change rates of CD4+ and CD8+ T lymphocytes were defined as the logarithm of the ratio of the value after 48 month to that at baseline. Comparison between groups was conducted using analysis of variance. Results The median of gene copy numbers of CCL3L1 and CCL4L were 2 (range: 0-8) and 3 (range: 0-7), respectively. After antiviral treatment, there were significantly different changes of CD8+ T lymphocyte level (F=3.054, P<0.05) and change rate of CD4+ /CD8+ (F=3.520, P<0.05) among groups of high (gene copy 4-8), median (gene copy 2-3) and low (gene copy 0-1) CCL3L1 gene copy numbers. The changes of CD8+ T lymphocyte levels (P=0.023) and change rates (P=0.038) in high and low CCL3L1 gene copy groups were both significantly different. There were significant differents changes rate of ratio of CD4+ /CD8+ T lymphocyte among high and median (P=0.010), high and low CCL3L1 gene copy numbers (F=4.397, P<0.05). The significant difference of the change rates of CD4+ /CD8+ were found between the gene copy 3 group and gene copy 4-7 group CCL4L (P=0.005) and between the gene copy 4-7 group and gene copy 0-2 group of CCL4L (P=0.030). The change ratio of CD4+ /CD8+ T lymphocytes increased with the increase of copy numbers of CCL4L gene. Conclusions The gene expressions of CCL3L1 and CCL4L might be associated with the ability of immune reconstitution of AIDS patients after antiretroviral therapy. Key words: Acquired immunodeficiency syndrome; Chemokine CCL3; Chemokine CCL4; Gene copy numbers; Immune reconstitution

Relationship between CCL20/CCR6/Th17 axis and vascular invasion and metastasis in patients with primary hepatocellular carcinoma

To investigate the role of CCL20/CCR6/Th17 axis in vascular invasion and metastasis of primary hepatocellular carcinoma (HCC). Expression levels of CCL20 mRNA in the normal human liver cell line L-02, and human hepatocellular carcinoma cell lines Hep3B, Huh7 and HepG2 were quantified by using SYBR green real time PCR. CCL20 secretions from these cell lines were quantified by using ELISA. The chemotactic effect of HCC cell line Hep3B on human peripheral blood mononuclear cells was determined by using transwell chemotaxis assay. Pre-therapy serum levels of IL-1α, IL-1β, IL-6, IL-8, IL-10, IL-17, IL-23, IFN-γ, TNF-α and CCL20 in 93 patients with HCC were measured by using 9-plex array and ELISA. All the patients were chronic hepatitis B virus associated HCC, and 51 cases were those with vascular invasion and metastasis (metastasis group) and 42 cases were not (non-metastasis group). CCL20 and CCR6 mRNA expressions in the HCC and tumor-adjacent tissues were determined by using SYBR Green real time PCR in 41 patients, among them, 20 cases were from the group of patients with metastasis and 21 cases were from the group of patients without metastasis. The CCL20 expression was further determined by immunohistochemistry. The HCC cell lines expressed and secreted higher amount of CCL20, which effectively recruited CCR6(+) T cells. Pre-therapy serum levels of CCL20 in 93 HCC patients were (38.2 ± 28.4)pg/ml, significantly increased than those with benign hepatic hemangiomas [(7.8 ± 17.8)pg/ml, P < 0.01]. In addition, the serum levels of CCL20 were positively correlated with the tumor diameters in HCC patients (r = 0.32, P = 0.0018). CCL20 was dominantly expressed in the cytoplasm in HCC cells, and it was also expressed by some infiltrating immune cells. The mRNA expression levels of CCL20 of the tumor tissues were significantly higher than that in the tumor-adjacent tissues (P < 0.05). Multivariate logistic regression analysis showed that serum levels of IL-17 and CCL20 were independent risk factors of metastasis in HCC patients (P < 0.05 for both). CCL20 mRNA showed no statistically significant differences between patients with metastasis and without metastasis in both tumor tissues and tumor-adjacent tissues (P > 0.05 for both). But the patients with metastasis showed significantly higher expressions of CCR6 both in their tumor [5.75 (1.79, 19.13)]and tumor-adjacent tissues [7.99 (4.49, 19.54)] than those with non-metastasis [1.69 (0.76, 2.87) and 3.58 (1.84, 4.32), P < 0.05 for both]. CCL20/CCR6/Th17 axis may promote vascular invasion and metastasis hepatocellular carcinoma.

Immunolocalization of CCL2-expressing cells in EAE and EAE-MSC cerebral cortex

The chemokine CCL2 has been considered as a mediator of inflammation in different diseases of the central nervous system, including experimental autoimmune encephalomyelitis (EAE), where the chemokine mediates extravasation of mononuclear leukocytes and loss of microvessel barrier function [1]. Previous studies have demonstrated that cellular sources of CCL2 during both EAE and multiple sclerosis (MS) are astrocytes and microvessel endothelial cells (ECs). Initially, we have demonstrated that in a MOG-induced model of EAE in C57BL/6 mice, 6 hrs after the intravenous treatment with bone marrow derived mesenchymal stem cells (MSCs) [2], the junctional staining patter of blood-brain barrier (BBB) microvessels and their functional effectiveness to permeability tracers seem to be restored. We have subsequently analysed, in the same experimental models, EAE and EAE-MSC mice, expression and immunolocalization of chemokine CCL2 by double immmunolabelling with cell-specific markers: endothelial PECAM-1 (CD31), OPCs (oligodendrocyte precursor cells) proteoglycan NG2, astrocytic GFAP, and Iba1 for microglia cells. Surprisingly, in the adopted model of cerebral cortex EAE, astrocytes and ECs do not show any detectable CCL2 expression, instead a strong staining is observed on activated parenchymal and perivascular microglia. Astrogliosis, microglia activation, and CCL2 overexpression appearing strongly reduced in EAE mice after MSC treatment. These observations identify microglia cells as the major source of CCL2 in EAE mice, whose barrier is damaged, and suggest the downregulation of the chemokine in perivascular microglia as a possible mechanism involved in BBB protection after MSC administration.

Immune mechanisms in acetaminophen-induced acute liver failure.

An overdose of acetaminophen (N-acetyl-p-aminophenol, APAP), also termed paracetamol, can cause severe liver damage, ultimately leading to acute liver failure (ALF) with the need of liver transplantation. APAP is rapidly taken up from the intestine and metabolized in hepatocytes. A small fraction of the metabolized APAP forms cytotoxic mitochondrial protein adducts, leading to hepatocyte necrosis. The course of disease is not only critically influenced by dose of APAP and the initial hepatocyte damage, but also by the inflammatory response following acetaminophen-induced liver injury (AILI). As revealed by mouse models of AILI and corresponding translational studies in ALF patients, necrotic hepatocytes release danger-associated-molecular patterns (DAMPs), which are recognized by resident hepatic macrophages, Kupffer cell (KC), and neutrophils, leading to the activation of these cells. Activated hepatic macrophages release various proinflammatory cytokines, such as TNF-α or IL-1β, as well as chemokines (e.g., CCL2) thereby further enhancing inflammation and increasing the influx of immune cells, like bone-marrow derived monocytes and neutrophils. Monocytes are mainly recruited via their receptor CCR2 and aggravate inflammation. Infiltrating monocytes, however, can mature into monocyte-derived macrophages (MoMF), which are, in cooperation with neutrophils, also involved in the resolution of inflammation. Besides macrophages and neutrophils, distinct lymphocyte populations, especially γδ T cells, are also linked to the inflammatory response following an APAP overdose. Natural killer (NK), natural killer T (NKT) and T cells possibly further perpetuate inflammation in AILI. Understanding the complex interplay of immune cell subsets in experimental models and defining their functional involvement in disease progression is essential to identify novel therapeutic targets for human disease.

Expression and clinical significance of CCL5 in patients with esophageal carcinoma

To investigate the expression and significance of CCL5 in patients with esophageal carcinoma. Using reverse transcriptase polymerase chain reaction (RT-PCR), the expressions of CCL5/CD8/granzyme B/perforin in tumor and corresponding adjacent tissues from esophageal carcinoma patients were examined. Flow cytometry (FACS) was used to detect the percentages of CD8(+) T cells and CCR5(+)CD8(+) T cells in TIL and PBMC from the patients. Transwell assay was performed to study the effect of CCL5 on the migration of T cells in vitro. T test and Spearman correlation analysis were performed. The mRNA expressions of CCL5 and perforin were 0.348 2 ± 0.300 1 and 0.181 9 ± 0.118 6, respectively, in the tumor samples, while their expressions in adjacent samples were 0.279 6 ± 0.138 0 and 0.118 0 ± 0.109 8, respectively, with no statistically significant differences between them (P > 0.05 for both). The mRNA expressions of CD8 and granzyme B were significantly higher in the tumor tissues than in adjacent tissues (0.464 9 ± 0.300 8 vs. 0.279 0 ± 0.173 4, 0.648 7 ± 0.516 0 vs. 0.469 7 ± 0.259 1; P < 0.05 for both). The relative expression of CCL5 was positively correlated with that of CD8, perforin and granzyme B (r(CD8) = 0.272, P = 0.034; r(perforin) = 0.305, P = 0.026; r(granzymeB) = 0.108, P = 0.012) in the tumor sites. FACS data revealed that the proportions of CD8(+) T cells in TIL and PBMC were (45.86 ± 16.09)% and (34.05 ± 15.07)%, respectively, showing a significant difference (P = 0.022). Similarly, CCR5(+)CD8(+) T cells fraction in TIL (48.12 ± 26.75)% was much higher than that in PBMC (19.53 ± 13.67) % (P < 0.001). Transwell assay showed that CCL5 protein enhanced the migration of T cells, supporting that CCL5 is crucial for CD8(+) T cells recruitment in vivo. Intriguingly, CCL5 expression was down-regulated in advanced patients (stage IIb-IV). The accumulation of CD8(+) T cells and CCR5(+)CD8(+) T cells was strongly reduced in advanced patients, suggesting that CCL5 expression may be involved in the local control of the disease and its reduction may be involved in disease progression. The current data indicate the involvement of CCL5 in the regulation of CD8(+) T cell entry into tumor lesions in esophageal carcinoma patients. This process may affect the disease status and potentially as a prognostic factor for cancer patients. Enhancing local CCL5 expression in tumor lesions may represent a novel strategy in esophageal cancer therapy.

Low-dose paclitaxel improves the therapeutic efficacy of recombinant adenovirus encoding CCL21 chemokine against murine cancer.

Secondary lymphoid tissue chemokine (SLC/CCL21), one of the CC chemokines, exerts potent antitumor immunity by co-localizing T cells and dendritic cells at the tumor site and is currently tested against human solid tumors. Here, we investigated whether the combination of recombinant adenovirus encoding murine CCL21 (Ad-mCCL21) with low-dose paclitaxel would improve therapeutic efficacy against murine cancer. Immunocompetent mice bearing B16-F10 melanoma or 4T1 breast carcinoma were treated with either Ad-mCCL21, paclitaxel, or both agents together. Our results showed that Ad-mCCL21 + low-dose paclitaxel more effectively reduced the growth of tumors as compared with either treatment alone and significantly prolonged survival time of the tumor-bearing animals. These antitumor effects of the combined therapy were linked to altered cytokine network at the tumor site, enhanced apoptosis of tumor cells, and decreased formation of new vessels in tumors. Importantly, the combined therapy elicited a strong therapeutic antitumor immunity, which could be partly abrogated by the depletion of CD4+ or CD8+ T lymphocytes. Collectively, these preclinical evaluations may provide a combined strategy for antitumor immunity and should be considered for testing in clinical trials.

Effects of maternal allergy symptoms on the cytokine level of umbilical cord blood of neonates

Objective To explore the effects of maternal allergy symptoms on the cytokine level of umbilical cord blood of neonates.Methods A cross sectional study was conducted among 136 pregnant women in Yiwu city from 1st July to 30th December,in 2012.A questionnaire on social economic charactertistics was used and blood sam-ple of pregnant women and umbilical cord blood sample were collected to detect the level of IgE,eosinophile granulo-cyte,Eotaxin,IL-9,IL-6,IL-4,IL-5,IFN-γ,IL-10.The differences between pregnant women with and without allergy symptoms were carried out.Results There were no significant differences in social and demographic characteristics between the two groups（all P〉0.05）.Pregnant women with allergy symptoms had higher IgE level（0.13 IU/mL vs 0.10 IU/Ml,Z=-2.063,P=0.039）,eosinophile granulocyte（0.39 ×109/mL vs 0.29 ×109/mL,Z=-2.548, P=0.011）,Eotaxin（66.18ng/L vs 48.35ng/L,Z=-2.144,P=0.032）,IFN-γ（927.81ng/L vs 338.65ng/L,Z=-2.051,P=0.040）,IL-10（15.59ng/L vs 11.55ng/L,Z=-2.022,P=0.043） than pregnant women without allergy symptoms in neonates′cord blood.Conclusion Maternal allergy symptoms may increase the level of IgE, eosinophile granulocyte,Eotaxin,IFN-γand IL-10 of neonates′cord blood. Key words: Anaphylaxis Fetal Blood Immunoglobulin E Cytokines

Chemokine CCL18 and tumor

Chemokine CCL18 plays significant roles in immune regulation by recruiting of inflammatory cells,which involves in immune and inflammatory processes.CCL18 protein is overexpressed in the serum of patients with cancer and some tumor tissues.However,it is still controversial that CCL18 plays the role of tumor promoter or tumor suppressor.Researches on the roles and mechanisms of CCL18 can provide new target for diagnosis and treatment of cancer. Key words: Chemotactic factors; Neoplasms; Receptors, chemokine