The aim of this study was to elucidate the comprehensive roles of cytokines in lung adenocarcinoma (LUAD). Cytokine-related genes were analyzed in LUAD using sequencing datasets from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO). Gene Set Variation Analysis (GSVA) was employed to quantify enrichment of four cytokine families—interferons (IFNs), tumor necrosis factors (TNFs), interleukins (ILs), and chemokines (CKs)—across samples. Differential expression and survival analyses assessed the impact of each family on LUAD prognosis. A prognostic model based on TNF family genes was constructed using the least absolute shrinkage and selection operator (LASSO) regression. Functional enrichment of the TNF Score (TNFS) was performed with ClusterProfiler. Finally, the role of the key gene TNFRSF11A was validated by small interfering RNA (siRNA) knockdown, followed by Transwell migration, colony formation, and wound-healing assays. Integrated expression and survival analyses identified the TNF family as a critical regulator in LUAD. TNF scores were significantly elevated in tumor versus normal tissues, whereas CK enrichment predicted improved survival and high TNF enrichment predicted poorer survival. Differential profiling in TCGA and GEO cohorts revealed five overexpressed TNF genes—TNFRSF11A, TNFRSF13B, TNFRSF17, TNFSF13, and TNFSF11—correlated with adverse outcomes. A five-gene LASSO-derived risk model demonstrated strong prognostic performance for overall, disease-free, disease-specific, and progression-free survival. High TNFS was associated with dysregulation of cell-cycle, adhesion, and cytokine signaling pathways, as well as altered infiltration of T cells, B cells, and macrophages. Single-cell analysis further revealed that malignant cells with high TNFRSF11A expression exhibited significantly enhanced intercellular communication with fibroblasts and CD8 + T cells, characterized by the activation of specific signaling pathways. TNFRSF11A emerged as the top contributor, with expression positively correlated with smoking history, advanced TNM stage, and recurrence. Functional assays confirmed that TNFRSF11A knockdown significantly impaired LUAD cell proliferation, migration, and invasion. The TNF cytokine family plays a pivotal role in LUAD. TNFRSF11A, previously unstudied in this context, represents a novel key driver of LUAD progression.

IntroductionLeprosy, a chronic infectious disease, is closely linked to the host immune response. According to the WHO, leprosy patients (L) and household contacts (HHC) are classified into subgroups: paucibacillary (PB) and multibacillary (MB), witch reflect the degree of infection in patients and the level of exposure of their contacts. The main goal of this study was to: i) establish a comprehensive overview of soluble mediator signatures of PBMCs upon in vitro antigen-specific stimuli and ii) identify whether the chemokine (CH) and cytokine (CY) signatures were associated with distinct clinical manifestations in (L) and immune response profiles in (HHC).MethodsLong-term PBMC cultures were carried out and supernatants collected for 12 CH and CY analisys by Cytometric Beads Array.Results and discussionThe CH and CY analysis, using continuous variable modeling, demonstrated that PBMCs from both L and HHC exhibited high levels of TNF upon M. leprae-stimuli. While lower production of IFN-γ were observed for L, low levels of CXCL8 was found for HHC. Soluble mediator signatures, analyzed using categorical variables, revealed that while high levels of TNF were observed for L, high levels of IFN-γ appeared as a hallmark of HHC. Overall, these analyses demonstrated that CXCL8, IFN-γ, and TNF were key markers differentiating L from HHC and endemic control (EC), especially considering the categorical analysis of the soluble mediator signatures. Data further demonstrated that higher levels of IFN-γ and lower levels CXCL8 was features associated with HHC(MB), whereas high levels of TNF were observed in both L subgroups. Moreover, data from integrative networks, based on correlation amongst soluble mediators, revealed that in M. leprae-stimuli, the number of correlations was lower in HHC(MB) compared to HHC(PB), but higher in L(MB) compared to L(PB). It was noted that the number of correlations decreased in the following order: EC > L > HHC. Our findings contribute to additional immunological features associated with L and HHC, witch can be useful complementary diagnostic/prognostic tools for classification of L and HHC, providing insights to enrich the research agenda about the hypothesis that HHC should be closely monitored as they may present a subclinical infection.

We recently reported that SARS-CoV-2 nucleocapsid (N) protein is abundantly expressed on the surface of both infected and neighboring uninfected cells, where it enables activation of Fc receptor-bearing immune cells with anti-N antibodies (Abs) and inhibits leukocyte chemotaxis by binding chemokines (CHKs). Here, we extend these findings to N from the common cold human coronavirus (HCoV)-OC43, which is also robustly expressed on the surface of infected and noninfected cells by binding heparan sulfate/heparin (HS/H). HCoV-OC43 N binds with high affinity to the same set of 11 human CHKs as SARS-CoV-2 N, but also to a nonoverlapping set of six cytokines. As with SARS-CoV-2 N, HCoV-OC43 N inhibits CXCL12β-mediated leukocyte migration in chemotaxis assays, as do all highly pathogenic and common cold HCoV N proteins. Together, our findings indicate that cell surface HCoV N plays important evolutionarily conserved roles in manipulating host innate immunity and as a target for adaptive immunity.

IntroductionImmune function in pregnancy is influenced by host-specific and environmental factors. This may impact fetal immune development, but the link between maternal and neonatal immune function is still poorly characterized. Here, we investigate the relationship between maternal and neonatal immune function, and identify factors affecting the association between maternal and child cytokine secretion.MethodsIn the French prospective cohort SEPAGES, blood samples were obtained from pregnant women (n=322) at gestational week 20 ± 4 and from their child at birth (n=156). Maternal and cord blood cytokine and chemokine (CK) levels were measured at baseline in all subjects and after T cell or dendritic cell activation with phytohemagglutinin or R848 (in total 29 and 27 measures in maternal and cord blood samples, respectively). Associations between environmental, individual factors and CK level were estimated by linear regression modeling. The maternal-cord blood CK relations were assessed by Pearson correlation and regression models.ResultsWe observed that pregnant women and neonates displayed specific CK secretion profiles in the innate and adaptive compartments at baseline and upon activation. Activation of T cells in cord blood induced high levels of IL-2, but low levels of IFNγ, IL-13 or IL-10, in comparison to maternal blood samples. Elsewhere, neonatal innate immune responses were characterized by low production of IFNα, while productions of IL-1β, IL-6, IL-8, IL-10 and TNFα were higher than maternal responses. Strong correlations were observed between most CK after activation in maternal and cord blood samples. Strikingly, a statistical association between global mother and child cytokine profiles was evidenced. Correlations were observed between some individual CK of pregnant women and their children, both at baseline (MCP1, RANTES) and after activation with R848 (IL-6, IL-8 and IL-10). We looked for factors which could influence cytokine secretion in maternal or cord blood, and found that leucocyte counts, maternal age, pre-conception BMI, smoking and season were associated with the levels of several CK in mothers or children. DiscussionOur study reveals in utero immune imprinting influencing immune responses in infants, opening the way to investigate the mechanisms responsible for this imprinting. Whether such influences have long lasting effects on children health warrants further investigation.

One of the main genetic factors of the development of atopic dermatitis (AD) in children are single nucleotide polymorphisms (SNP) of the filagrin gene (FLG), particularly rs_7927894 FLG. One of the mostly studied and promising AD marker chemokines (CK) is the thymusE and activation regulated chemokine (TARC/CCL17). Purpose – to detect the associations and role of different variants of SNP rs_7927894 FLG gene and TARC/CCL17 in children suffering different AD clinical proE files (CP) – isolated or combined with comorbid atopic disorders (AtD). Materials and methods. The main group comprised 39 patients aged 3 to 18 years, suffering the isolated AD or combined with comorbid AtD. The control group comprised 47 patients aged 3 to 18 years, suffering the pathology of gastrointestinal tract without clinical signs of atopy. All the patients of the main and control groups had undergone detection of the genotype variants of SNP rs_7927894 FLG gene by real-time polymerase chain reaction and detection of TARC/CCL17 serum concentrations in venous blood. The cutEoff value of statistical significance was set as p<0.05. Results. The incidence and association of genotype variants C/C, C/T and T/T SNP rs_7927894 FLG gene in patients of cohorts of the studied groups were detected as follows: C/T rs_7927894 FLG was significantly the most common in the general main group (56.4%, p<0.05), within the cohort of CP AD isolated (61.1%, p<0.05) and CP of AD combined with comorbid AtD (52.4%, p<0.05). There were detected the associations of studied SNP with AD: C/T rs_7927894 FLG is significantly directly associated with AD (r=0.291, p<0.05), C/C rs_7927894 FLG has a reverse association with a trend to significance (r=-0.194, p=0.07). Mean serum concentrations of TARC/CCL17 did not differ significantly among patients cohorts of the main and control groups, respectively: general main group — 615.8 pg/ml, main with a CP AD isolated — 651.3 pg/ml, main with a CP of AD combined with comorbid AtD — 585.4 pg/ml, control — 608.4 pg/ml (p>0.05). Associations of serum TARC/CCL17 concentrations were determined as follows: elevation trending to significance within increasing AD severity degree (r=0.290, p=0.07) and significant elevation within the AD exhacerbation period (r=0.426, p<0.05). No significant association of TARC/CCL17 as to AD patients compared to the control group was detected in our study (r=-0.027, p>0.05). Conclusions. The genotype heterozygote variant C/T rs_7927894 FLG is significantly the most common and associated with all AD CP in children — isolated and combined with comorbid AtD. Variant C/C rs_7927894 of FLG gene is significantly reversely associated with AD in children. Serum concentrations of TARC/CCL17 did not reveal any significant differences between the AD patients and nonEatopic ones. However, they significantly elevate within AD exacerbation phase and trending to significance within AD severity degree increase in children. The research was carried out in accordance with the principles of the Helsinki declaration. The study protocol was approved by the Local Ethics Committee of all participating institutions. The informed consent of the patient was obtained for conducting the studies. No conflict of interest was declared by the authors. Key words: atopic dermatitis, children, associations, polymorphism, filaggrin, thymus- and activation regulated chemokine.

Chemokines (CKs) are key players of immune-cell homing and differentiation. CK receptors (CKRs) can be used to define T-cell functional subsets. We aimed to characterize the CKR profile of the regulatory B-cell subset B10+ cells and investigate the CKs involved in their migration and differentiation in healthy donors and patients with RA. RNA sequencing and cytometry were used to compare CKR expression between B10+ and B10neg cells. Migration of B10+ and B10neg cells and IL-10 secretion of B cells in response to recombinant CKs or synovial fluid (SF) were assessed. CXCR5 was expressed at a higher level on the B10+ cell surface as compared with other B cells (referred to as B10neg cells). In line with this, its ligand CXCL13 preferentially attracted B10+ cells over B10neg cells. Interestingly, synovial fluid from RA patients contained high levels of CXCL13 and induced strong and preferential migration of B10+ cells. Besides its role in attracting B10+ cells, CXCL13 also promoted IL-10 secretion by B cells. In RA patients, the level of CXCR5 on B-cell surface was reduced. The preferential migration of RA B10+ cells toward CXCL13-rich SF was lost and CXCL13 stimulation triggered less IL-10 secretion than in healthy donors. Our results identify that the CXCR5/CXCL13 axis is essential for B10+ cell biology but is defective in RA. Restoring the preferential migration of B10+ within the affected joints to better control inflammation may be part of the therapeutic approach for RA.

From Bone Marrow to Skin: The Transient Increase in Circulating Endothelial Progenitor Cells in Patients with Superficial and Full Thickness Burns Correlates with Surface Area and Depth of Injury and Circulating Chemokine Levels.

Plants and natural compounds are extensively reported for diverse biological activities, including their effects on the inflammation pathway. The annual winter herb Diplotaxis Acris (D.Acris) is found only slopes of sandy and stony valleys in the desert. This research is intended to make a contribution to the literature regarding the employment of the species of plant ethnomedicinally by undertaking FTIR spectroscopic analysis and examining several concentrations of the plant's extract for anti-inflammatory activity in vitro with activated THP-1 human macrophages to examine its mediating effect on inflammation. Cell viability was also evaluated, and there was no severe cytotoxic effect from D.Acris extract with any of the concentrations being assessed on cells. ELISA was used to assess the pro-inflammatory cytokines and chemo kines that were produced. It has been noted that the plant extract led to a significant decrease in levels of the pro-inflammatory cytokines, including interleukin (IL)-1β, tumour necrosis factor (TNF)- α and IL-6. Inhibition of pro-inflammatory cytokines indicates the anti-inflammatory trends of D.Acris. This plant can be investigated further by isolation of natural compounds from the extract and effects of these compounds can be evaluated on the same inflammatory markers to show the main active constituent responsible for anti-inflammatory activities.

Background Hormonal changes during the menstrual cycle appear to play a key role in shaping immunity in the cervicovaginal tract and may influence the risk of sexually transmitted infections. Cervicovaginal fluid contains cytokines, chemokines, immunoglobulins, and other immune mediators. Many studies have shown that the concentrations of these immune mediators change throughout the menstrual cycle but have often shown conflicting results. Thus, our understanding of the immunological correlates of the menstrual cycle remains vague and could be improved by a meta-analysis of all available data sets. Results We present a protocol for a systematic review and meta-analysis of individual participant data of cervicovaginal immune mediators during the menstrual cycle. Our primary objective is to estimate the differences in concentrations of immune mediators between the follicular and luteal phases of the menstrual cycle. Our secondary objectives are to compare how four technical factors (sample type, assay type, method of determining menstrual cycle phase, and normalization of immune mediator concentrations to total protein) affect the estimated differences across the menstrual cycle phases. In addition to summarizing previous studies, we will perform a new study, measuring select immune mediators in 200 paired cervicovaginal lavage samples. This additional study will strengthen the evidence and test the validity of the meta-analysis. Conclusions Our systematic review and meta-analysis will provide precise estimates of immune mediator concentrations throughout the menstrual cycle. This improved understanding of cervicovaginal immunity across the menstrual cycle will provide important baseline knowledge for the design of clinical trials of vaginal interventions, including hormonal contraception and prevention tools for sexually transmitted infections.

Cytokines and chemokines are engaged in the protection of an organism against external aggressors and diseases. They work together regulating and determining the nature of immune responses and controlling the immune cell trafficking and the cellular arrangement of immune organs.

Diabetic nephropathy is a serious complication of diabetes up to development of terminal renal failure with a high mortality rate. It is important to realize that in its pathogenesis there is accumulation of various pro-inflammatory cytokines, chemokines, adhesion molecules, uric acid and glycated hemoglobin, as well as oxidative stress with increased activity of the renin-angiotensin-aldosterone system. In this case there is thickening of the glomerular basement membrane, mesangial expansion, nodular glomerular sclerosis, and tubulointerstitial fibrosis. Treatment is mainly based on the control of sugar levels and blood pressure and there is practically no validated therapy that can stop the kidney damage progression. Therefore, in all these cases, plasmapheresis is almost the only and pathogenetically justified method of treating and preventing this condition. Only plasmapheresis can remove numerous damaging factors, such as circulating immune complexes (CIC), glycoproteins, lipids, uric acid, endothelin, antibodies to insulin and others.

The amyloid precursor protein plus presenilin-1 (APP/PS1) mice are a frequently-used model for Alzheimer’s disease studies (AD). Using behavioral studies, quantitative RT-PCR and Western-blot techniques, significant findings were determined by the expression of proteins involved in inflammation comparing APP/PS1 and Wild type mice. Increased GFAP expression could be associated with the elevation in number of reactive astrocytes. IL-3 is involved in inflammation and ABDF1 intervenes normally in the transport across cell membranes and both were found up-regulated in APP/PS1 mice compared to Wild type mice. We noted for the first time, a CCR8 increase expression with diminution of its CCL1 chemokine, both normally involved in protection from bacterial infection and demyelination. Furthermore, CCR5 expression was decreased and both CCL3 and CCL4 chemokines were highly expressed indicating a possible gliosis and probably an increase in chemotaxis from lymphocytes and T cell generation. Inflammation in AD will be the next step in the therapeutic approach.

THU0050 CXCL13 IS A KEY DRIVER FOR MIGRATION AND DIFFERENTIATION OF REGULATORY B CELLS

OPINION article Front. Immunol., 15 May 2020Sec. Cytokines and Soluble Mediators in Immunity Volume 11 - 2020 | https://doi.org/10.3389/fimmu.2020.00908

Non-small cell lung cancer (NSCLC) accounts for the majority of lung cancer, with an unfavorable prognosis of 5-year survival rates. It is of great clinical significance to further search for more efficacious and novel targets for diagnosis and therapeutic strategies. This study aimed at clarifying the role of long non-coding RNA (lncRNA) NORAD in proliferation, invasion and migration and tumor growth of NSCLC. In this study, mRNA levels of lncRNA NORAD were examined by RT-PCR. CCK-8 assay was applied to test cell viability. Furthermore, wound healing assay and transwell assay were performed to detect the migration and invasion of A549 cells, respectively. Immunohistochemistry was applied to assess the levels of CXC chemokine receptor (CXCR) 4 and CXC chemokine ligand (CXCL) 12. Mice models of NSCLC in vivo were exploited to further examine the potential role of NORAD in tumor growth. Key proteins related to Ras homolog gene family member A (RhoA) GTPase/Rho-associated kinase (RhoA/ROCK) pathway were determined by Western blot. NORAD has elevated the levels in NSCLC tissues and cells. NORAD interference dramatically inhibited tumor growth and suppressed A549 cell proliferation, migration and invasion by downregulating CXCR4 and CXCL12 expression. RhoA/ROCK signaling pathway was activated in NSCLC. This study revealed that the downregulation of lncRNA NORAD could slow down the progression of NSCLC by regulating CXCR4 and RhoA/ROCK signaling pathway.

Allergic bronchopulmonary aspergillosis (ABPA) is a severe lung disease caused by hypersensitivity to Aspergillus spp. The search for new diagnostic markers is essential for early detection of the disease in patients at risk and identifying eff ective treatment strategies. 21 patients with ABPA, 37 patients with asthma and 16 healthy subjects were examined. The content of thymic stromal lymphopoietin (TSLP), thymus-associated regulatory chemokine (TARC), IL-8, eosinophil count, total IgE levels and specifi c IgE to Aspergillus fumigatus were determined in serum by ELISA. The positive correlation of the TARC level with the indicators of total IgE, sIgE to Aspergillus fumigatus, the number of eosinophils and the negative correlation relationship with the FEV1 value confi rms the important diagnostic value of this pro-infl ammatory chemokine in patients with ABPA.

At present, since the mechanism of occurrence and development of bone cancer pain (BCP) is sophisticated, it is still perplexing in the clinical practice. MicroRNA (miRNA), which plays a regulatory role at the post-transcriptional level, may be in-volved in the BCP process. Therefore, the search for unique miRNA and biomarkers involved in the occurrence and development of BCP will be helpful for the treatment, clinical detection and diagnosis. In this paper, we reviewed recent researches and described how miRNA regulate osteoclast activation, promoted bone resorption and led to the formation of BCP. We also described how miRNA regu-late different signaling pathways [chemokine C-X-C motif ligand 12 (CXCL12)/chemokine C-X-C motif receptor 4 (CXCR4) signaling pathway, protein kinase A/cAMP-response element binding protein (CREB) signaling pathway, et al] that involved in the formation and development of BCP and how miRNA plays a role in BCP regulation by regulating neuronal plasticity and changing the expression of neuronal ion channels. Subsequently, This review summarizes the occurrence and development mechanism of BCP and provides help for clinical transformation. Key words: MicroRNA; Bone cancer pain; Osteoclast

Objective To observe the preventive effects of infliximab in autoimmune hepatitis (AIH) and to explore its mechanism. Methods The mice AIH model was established by injecting concanavalin A (Con-A) into the caudal vein. Forty mice were divided into prevention group and control group, with 20 mice in each group. The mice of prevention group were injected intravenously with infliximab (20 mg/kg) one hour before Con-A injection and the mice of control group were administrated with 200 μL phosphate buffered saline (PBS). Serum was collected 3, 8, 12 and 24 h after Con-A/PBS injection. The serum level of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) was detected by colorimetry. The level of cytokine interleukin (IL)-6, IL-1β, interferon gamma (IFN-γ), IL-4, IL-17A, IL-10 and chemokine C-X-C motif ligand 10 (CXCL10) was measured by enzyme-linked immunosorbent assay (ELISA). Liver samples were taken 12 h after Con-A/PBS injection for hematoxylin-eosin staining. Liver infiltrated lymphocytes were assessed by flow cytometry. The expression of T-box transcription factor 21 (TBX21), GATA binding protein 3 (GATA3), RAR related orphan receptor C (RORC) and CXCL10 at mRNA level was evaluated by quantitative real-time polymerase chain reaction (qRT-PCR). The expression of CXCL10 in liver was detected by Western blotting. Paired t test and one-way analysis of variance were used for statistic analysis. Results At 8, 12, and 24 h after Con-A injection, the serum ALT level, AST level, IL-1β and IFN-γ of prevention group were all lower than those of control group ((545.8±190.3) U/L vs. (865.8±237.7) U/L, (947.6±267.9) U/L vs. (1 448.0±403.5) U/L, (508.6±131.1) U/L vs. (976.6±207.6) U/L; (620.7±132.0) U/L vs. (952.9±106.8) U/L, (801.6±212.0) U/L vs. (1 424.8±236.0) U/L, (632.1±117.8) U/L vs. (1 008.3±187.5) U/L; (31.38±10.12) ng/L vs. (48.12±11.53) ng/L, (39.34±11.40) ng/L vs. (60.00±14.17) ng/L, (29.49±8.22) ng/L vs. (46.89±5.50) ng/L; and (432.93±66.82) ng/L vs. (674.66±97.88) ng/L, (655.09±169.17) ng/L vs. (937.90±166.36) ng/L, (263.40±54.97) ng/L vs. (410.74±86.64) ng/L), and the differences were statistically significant (t = 2.350, 2.308, 4.263, 4.374, 4.860, 3.806, 2.440, 2.541, 3.939, 4.560, 2.660 and 3.210; all P 0.05). Conclusions Infliximab has certain preventive effects in mice AIH model, which may be achieved by antagonizing TNF-α and decreasing the expression of CXCL10 in liver, reducing the infiltration of T-helper 1 cells and CD8+ T cells into liver, and by reducing T lymphocyte activation induced by inflammatory cytokines thus alleviating the damage of T lymphocytes to hepatocytes. Key words: Hepatitis, autoimmune; Infliximab; C-X-C motif chemokine ligand 10; Mice

In recent years, with the increasing incidence of diabetes, diabetic keratopathy has gradually attracted more attention from clinicians.Diabetic keratopathy is mainly manifested as delayed corneal epithelial healing, corneal edema, decreased corneal sensitivity, and neurotrophic corneal ulcer.There are many mechanisms of diabetic keratopathy, including the abnormal accumulation of metabolites, an inflammatory reaction, oxidative stress, the lack of neurotrophic factors, corneal limbal stem cell abnormalities, etc.At present, most of the research on diabetic keratopathy at home and abroad has mainly focused on epithelial damage repair and changes in nerve function, and the pathological mechanism is mainly inflammatory response and apoptosis.Nuclear factor kappa B(NF-κB) is an important transcription regulatory factor, and is involved in regulating the expression of inflammatory factors, chemokines, cell adhesion molecules, apoptosis-related genes, growth factors, and other target genes.Studies have reported that chronic inflammation and epithelial cell apoptosis of the diabetic corneal epithelium are involved in the regulation of the NF-κB signaling pathway, which is also involved in the regulation of diabetic peripheral neuropathy, and diabetic corneal neuropathy belongs to the category of diabetic peripheral neuropathy.The NF-κB signaling pathway is closely related to the occurrence and development of diabetic keratopathy, and this article summarizes its mechanism. Key words: Diabetes mellitus/complications; Diabetic keratopathy; Nuclear factor-κB; Mechanism; Singnal pathway

Objective To investigate the expression of interleukin-10 (IL-10) and chemokine receptor 7 (CXCR7) in papillary thyroid carcinoma (PTC) tissues and their correlation with invasion and metastasis. Methods According to the inclusion and exclusion criteria, 68 cases of cancer tissues (cancer tissue group) and para-cancer tissues (para-cancer tissue group) collected from PTC patients in Wenzhou Hospital of Traditional Chinese Medicine from Jun. 2015 to Jun. 2018 were selected. Meanwhile, pathological specimens from 32 cases of thyroid follicular adenoma patients (thyroid follicular adenoma group) undergoing thyroidectomy during the same period were also enrolled. Immunohistochemical SP staining was used to observe the expression of IL-10 and CXCR7 in different tissues, and the correlation between the expression of IL-10 and CXCR7 and the pathological characteristics of tumor was analyzed. Results The positive expression rates of IL-10 and CXCR7 in cancer tissues were significantly higher than those in para-cancer tissues and thyroid follicular adenoma group (88.24% vs. 14.71% vs. 0.00%, 75.00% vs. 32.35% vs. 15.63%; P<0.05) . Among 68 PCT patients, 38 (55.88%) had high expression of IL-10, 30 (44.12%) had low expression of IL-10, 32 (47.06%) had high expression of CXCR7, and 36 (52.94%) had low expression of CXCR7. IL-10 expression was positively correlated with tumor multifocal, TNM stage, central lymphatic metastasis, central + cervical lymphatic metastasis, invasion degree and tumor maximum diameter (r=0.486, 0.509, 0.468, 0.422, 0.629, 0.674, P<0.05) . CXCR7 expression was positively correlated with tumor multifocal, TNM staging, central lymphatic metastasis, central + cervical lymphatic metastasis, and infiltration (r=0.425, 0.563, 0.490, 0.287, 0.481, P<0.05) . Conclusions IL-10 and CXCR7 are highly expressed in cancer tissues of PTC patients, among which IL-10 expression level is closely related to tumor differentiation degree, TNM stage, cervical lymphatic metastasis, infiltration degree and tumor maximum diameter. CXCR7 is related to TNM stage, cervical lymphatic metastasis and infiltration degree, both of which may be involved in the occurrence and development of tumor. Key words: IL-10; CXCR7; Papillary thyroid carcinoma; Invasion; Central lymphatic metastasis; Cervical lymphatic metastasis